A. Distler

SYMPATHETIC NERVOUS SYSTEM AND BLOOD-PRESSURE CONTROL IN ESSENTIAL HYPERTENSION

In normotensive subjects an inverse correlation was observed between an index of sympathetic nervous activity (the plasma-noradrenaline concentration during physical exercise) and reactivity to exogenous noradrenaline. This relationship was invariably disturbed in age-matched patients with essential hypertension. Multiple-regression analysis revealed a highly significant correlation between the combination of both factors and the height of mean arterial blood-pressure (r=0.91). The findings suggest that sympathetic nervous activity and pressor response to noradrenaline together form an important determinant of the arterial blood-pressure level. An inverse relationship could be demonstrated between plasma-renin concentration and pressor response to angiotensin II in normotensives, and this relationship was unchanged in hypertensive patients. Therefore angiotensin II does not appear to contribute directly to high blood-pressure.

The Effect of Tyramine, Noradrenaline, and Angiotensin on the Blood Pressure in Hypertensive Patients with Aldosteronism and Low Plasma Renin*

Abstract The reactivity to the pressor action of tyramine, noradrenaline, and angiotensin was determined in 9 patients with hypertension, aldosteronism and low plasma renin concentration (4 patients with solitary adrenal adenomas, 3 patients with nodular adrenal hyperplasia, 2 patients with unknown adrenal status). In 7 patients tests were repeated following unilateral or subtotal adrenalectomy respectively. For comparison, 5 patients with phaeochromocytoma, 10 patients with benign essential hypertension, and 12 normotensive control subjects were studied. — In the hypertensive patients with aldosteronism and low plasma renin, responsiveness to tyramine was significantly reduced. In contrast, pressor response to noradrenaline was in the normal range, and sensitivity to angiotensin was increased. Following adrenal surgery, sensitivity to tyramine increased in all cases but one, sensitivity to noradrenaline did not change significantly, and responsiveness to angiotensin decreased in all cases but one. — It is discussed that the reduced pressor effect of tyramine in the hypertensive patients with aldosteronism is due to a disturbance of adrenergic function which may be of importance for the diminished production of renin in these forms of hypertension.

Hochdruck und Aldosteronismus bei solitären Adenomen und bei nodulärer Hyperplasie der Nebennierenrinde

Zusammenfassung1. Es wird über 10 Patienten mit Hypertonie und vermehrter Aldosteronbildung berichtet, bei denen unter dem Verdacht eines hypobzw. normokaliämischen primären Aldosteronismus eine chirurgische Exploration der Nebennieren vorgenommen wurde. Bei der Operation fanden sich nur in 5 Fällen (4 Frauen, 1 Mann) solitäre bzw. maximal 2 Nebennierenrindenadenome, bei den übrigen Patienten (4 Männer, 1 Frau) wurde eine noduläre Nebennierenrindenhyperplasie festgestellt.2. Für die differentialdiagnostische Entscheidung, ob der Aldosteronismus durch ein solitäres Adenom oder durch eine noduläre Hyperplasie der Nebennierenrinden verursacht wurde, erwies sich die Bestimmung der Plasmareninkonzentration als ungeeignet. Sowohl bei den 5 Patienten mit klassischem primärem Aldosteronismus als auch bei 4 Patienten mit nodulärer Nebennierenrindenhyperplasie wurden wechselnd erniedrigte und im Normbereich liegende Plasmareninwerte gefunden. Nur bei einem Patienten mit knotiger Umwandlung der Nebennierenrinde waren die Reninwerte konstant normal.3. Die Patienten mit echtem primärem Aldosteronismus bei solitären bzw. maximal 2 Nebennierenrindenadenomen wiesen ausnahmslos das typische klinische Bild des Conn-Syndroms mit leichter bis mittelschwerer Hypertonie bei ausgeprägter Hypokaliämie und erhöhtem Blutvolumen auf. Bei 4 Patienten mit nodulärer Nebennierenrindenhyperplasie war die Hypertonie wesentlich schwerer als bei den Fällen mit solitären Adenomen. Eine ausgeprägte Hypokaliämie bestand lediglich in einem Fall; bei den übrigen Patienten war das Serumkalium nur leicht erniedrigt oder normal. — Nach diesen Befunden scheint insbesondere das Vorliegen einerschweren Hypertonie beinormalem oder nurleicht erniedrigtem Serumkalium und fehlender Erhöhung des Blutvolumens ein solitäres Adenom der Nebennierenrinde als Ursache eines Hochdrucks mit Aldosteronismus unwahrscheinlich zu machen.4. Mindestens bei 3 der Patienten mit nodulärer Nebennierenrindenhyperplasie, die eine schwere Hypertonie bei normalem oder nur leicht erniedrigtem Serumkalium aufwiesen, kann der Aldosteronismus nicht als Hochdruckursache angesehen werden; dieser dürfte sich vielmehr erst sekundär im Verlauf einer wahrscheinlich essentiellen Hypertonie entwickelt haben.Summary1. 10 patients with hypertension and increased aldosterone production are described, who underwent adrenal surgery because hypo- or normokalemic primary aldosteronism was suspected. At operation, only in 5 cases (4 females, 1 male) solitary or maximally 2 adrenal adenomas were found, in the other patients (4 males, 1 female) nodular adrenal hyperplasia was detected.2. In deciding, whether or not aldosteronism was caused by a solitary adenoma or by nodular adrenal hyperplasia, determination of plasma renin concentration did not prove to be useful. In the 5 patients with classic primary aldosteronism as well as in 4 patients with nodular adrenal hyperplasia plasma renin concentrations ranging between suppressed and normal values were observed. Only in 1 patient with nodular adrenal hyperplasia plasma renin values were consistently normal.3. The patients with classic primary aldosteronism due to solitary or maximally 2 adrenal adenomas showed the typical clinical symptoms of Conns syndrome, i.e. slight to moderate hypertension, pronounced hypokalemia and increased blood volume. In 4 patients with nodular adrenal hyperplasia hypertension was much more severe than in the cases with solitary adenomas. Marked hypokalemia was observed only in 1 case; in the others serum potassium was either just slightly decreased or normal. — These findings suggest that aldosteronism is unlikely to be caused by a solitary adrenal adenoma when the combination of severe hypertension with normal or just slightly decreased serum potassium and lacking hypervolemia is encountered.4. At least in 3 of the patients with nodular adrenal hyperplasia who exhibited severe hypertension together with normal or just slightly decreased serum potassium values, aldosteronism cannot be considered the cause of high blood pressure. It seems likely that aldosteronism in these cases was not primary but secondary, originating from advanced essential hypertension.

Tagesprofile von Plasmaaldosteron,-Cortisol, -Renin, -Angiotensinogen und -Angiotensinasen bei Normalpersonen

SummaryPlasma cortisol and renin were estimated in 1 h intervals, plasma aldosterone, angiotensinogen and angiotensinases in 3 h intervals over periods of 24 h in six normal volunteers (age 20–26) under control conditions and subsequently under suppression of ACTH released by dexamethasone.Highest cortisol levels were found around 7 a.m., minimum levels between 9 p.m. and 1 a.m. Dexamethasone reduced cortisol to constantly low concentrations.Aldosterone was highest around 4 a.m. under control conditions and under dexamethasone, and showed lowest concentrations between 4 and 10 p.m. There were no significant differences between mean aldosterone concentrations at corresponding time points of the control and the dexamethasone period.Similar to aldosterone, renin showed peak values around 4 a.m. All mean values at corresponding time points between 7 a.m. and 11 p.m. and the 24 hour mean values of each subject were significantly increased under the influence of dexamethasone.No evidence could be achieved for the existence of circadian rhythms of angiotensinogen and angiotensinases. Dexamethasone did not cause significant changes of these parameters.The data suggest that circadian rhythms of aldosterone and renin are similar to each other but not exactly synchronized to that of cortisol. When ACTH release is inhibited by dexamethasone renin increases to maintain normal aldosterone levels. Angiotensinogen and angiotensinases, parameters which may influence the active concentration of angiotensin II, do not seem to be involved in the regulation of aldosterone.ZusammenfassungAn 6 normalen männlichen Freiwilligen im Alter von 20–26 Jahren wurden Plasmacortisol und -renin stündlich, Plasmaaldosteron, -angiotensinogen und -angiotensinasen alle 3 Std über jeweils 24 Std unter Kontrollbedingungen und anschließend unter Suppression der ACTH-Freisetzung durch Dexamethason gemessen.Die höchsten Cortisolspiegel fanden sich gegen 7 Uhr, die niedrigsten zwischen 21 und 1 Uhr. Die Gabe von Dexamethason führte zu konstant niedrigen Cortisolkonzentrationen.Aldosteron war unter Kontrollbedingungen und unter Dexamethason gegen 4 Uhr am höchsten und zeigte niedrigste Werte zwischen 16 und 22 Uhr. Zwischen den mittleren Aldosteronkonzentrationen entsprechender Zeitpunkte der Kontroll- und der Dexamethasonperiode bestanden keine signifikanten Unterschiede.Ähnlich dem Aldosteron zeigte das Plasmarenin Maximalwerte gegen 4 Uhr. Alle Mittelwerte entsprechender Zeitpunkte zwischen 7 und 23 Uhr und die jeweiligen 24 Std-Mittelwerte jedes einzelnen Probanden waren unter dem Einfluß von Dexamethason signifikant erhöht.Für die Existenz circadianer Rhythmen des Angiotensinogens und der Angiotensinasen konnte kein Anhalt gewonnen werden. Dexamethason bewirkte keine signifikanten Veränderungen dieser Parameter.Die Ergebnisse deuten darauf hin, daß die circadianen Rhythmen von Aldosteron und Renin miteinander vergleichbar, jedoch nicht exakt mit dem des Cortisols synchronisiert sind. Unter der Hemmung der ACTH-Freisetzung durch Dexamethason steigt die Reninaktivität an, der Aldosteronspiegel bleibt unverändert. Angiotensinogen und die Angiotensinasen, Parameter, die die aktive Konzentration des Angiotensin II beeinflussen können, scheinen an der Regulation des Aldosterons nicht beteiligt zu sein.Plasma cortisol and renin were estimated in 1 h intervals, plasma aldosterone, angiotensinogen and angiotensinases in 3 h intervals over periods of 24 h in six normal volunteers (age 20-26) under control conditions and subsequently under suppression of ACTH release by dexamethasone. Highest cortisol levels were found around 7 a.m., minimum levels between 9 p.m. and 1 a.m. Dexamethasone reduced cortisol to constantly low concentrations. Aldosterone was highest around 4 a.m. under control conditions and under dexamethasone, and showed lowest concentrations between 4 and 10 p.m. There were no significant differences between mean aldosterone concentrations at corresponding time points of the control and the dexamethasone period. Similar to aldosterone, renen showed peak values around 4 a.m. All mean values at corresponding time points between 7 a.m. and 11 p.m. and the 24 hour mean values of each subject were significantly increased under the influence of dexamethasone. No evidence could be achieved for the existence of circadian rhythms of angiotensinogen and angiotensinases. Dexamethasone did not cause significant changes of these parameters.

Renales Kallikrein-Kinin-System und Blutdruckregulation

Kallikrein excreted with the urine appears to be formed in the kidney. The kallikrein-kinin system in the kidney is localized in the distal nephron from the juxtaglomerular apparatus to the collecting duct. It has been shown that intrarenal infusion of kinins produces an increase in renal blood flow as well as diuresis and natriuresis. Part of the effect of kinins appears to be mediated by the release of prostaglandins. However, the precise role of the renal kallikrein-kinin system in sodium and volume homeostasis and in blood pressure regulation still remains to be determined. Mineralocorticoids as well as the diuretics furosemide, bumetanide and bendroflumethiazide increase, spironolactone decreases kallikrein excretion. Urinary kallikrein has been shown to increase acid-as well as cryoactivation of prorenin in vitro. It is unclear as yet, however, whether the renal kallikrein-kinin system takes part in converting inactive prorenin into active renin in vivo. There are reports on subnormal, normal as well as increased kallikrein excretion in spontaneously hypertensive rats. In rats susceptible to the hypertensive effect of salt a substantially decreased excretion of kallikrein has been observed. Kallikrein excretion has been described to be increased in primary aldosteronism and to be reduced in a proportion of patients with established essential hypertension. In patients with labile hypertension, however, kallikrein excretion appears to be normal suggesting that decreased urinary kallikrein in essential hypertension is a consequence rather than a cause of hypertension. The renal kallikrein-kinin system does not appear to play a primary role in the pathogenesis of hypertension.SummaryKallikrein excreted with the urine appears to be formed in the kidney. The kallikrein-kinin system in the kidney is localized in the distal nephron from the juxtaglomerular apparatus to the collecting duct. It has been shown that intrarenal infusion of kinins produces an increase in renal blood flow as well as diuresis and natriuresis. Part of the effect of kinins appears to be mediated by the release of prostaglandins. However, the precise role of the renal kallikrein-kinin system in sodium and volume homeostasis and in blood pressure regulation still remains to be determined. Mineralocorticoids as well as the diuretics furosemide, bumetanide and bendro-flumethiazide increase, spironolactone decreases kallikrein excretion. Urinary kallikrein has been shown to increase acid-as well as cryoactivation of prorenin in vitro. It is unclear as yet, however, whether the renal kallikrein-kinin system takes part in converting inactive prorenin into active renin in vivo.There are reports on subnormal, normal as well as increased kallikrein excretion in spontaneously hypertensive rats. In rats susceptible to the hypertensive effect of salt a substantially decreased excretion of kallikrein has been observed. Kallikrein excretion has been described to be increased in primary aldosteronism and to be reduced in a proportion of patients with established essential hypertension. In patients with labile hypertension, however, kallikrein excretion appears to be normal suggesting that decreased urinary kallikrein in essential hypertension is a consequence rather than a cause of hypertension. The renal kallikrein-kinin system does not appear to play a primary role in the pathogenesis of hypertension.ZusammenfassungDas mit dem Urin ausgeschiedene Kallikrein scheint in der Niere gebildet zu werden. Hauptbildungsort von Kallikrein in der Niere ist das distale Tubulussystem vom juxtaglomerulären Apparat bis zu den Sammelrohren. Die Infusion von Kininen in die Nierenarterie führt zu einer Zunahme des renalen Blutflusses sowie zur Diurese und Natriurese, wobei ein Teil der Wirkung der Kinine offenbar durch Prostaglandine vermittelt wird. Bisher ist jedoch nicht klar, welche physiologische Wirkung dem Kallikrein-Kinin-System für die Natrium- und Volumenhomöostase bzw. für die Blutdruckregulation zukommt. Die Bildung und Ausscheidung von Kallikrein wird durch Mineralocorticoide gesteigert und durch Spironolactone vermindert. Die Diuretika Furosemid, Bumetanid und Bendroflumethiazid steigern die Kallikrein-ausscheidung. Urin-Kallikrein ist in vitro in der Lage, die Säure- und Kryoaktivierung von inaktivem Renin zu beschleunigen. Es ist jedoch noch unklar, ob Nierenkallikrein eine physiologische Rolle bei der Umwandlung von inaktivem Prorenin in enzymatisch aktives Renin spielt.Bei spontan hypertensiven Ratten wurde sowohl eine erniedrigte, eine normale wie eine erhöhte Kallikrein-Ausscheidung beschrieben. Ratten, die aufgrund einer genetisch bedingten Empfindlichkeit gegenüber Kochsalz unter gesteigerter Natriumzufuhr eine Hypertonie entwickeln, weisen eine stark erniedrigte Kallikrein-Ausscheidung auf. Bei Patienten mit primärem Aldosteronismus liegt eine erhöhte, bei einem Teil der Patienten mit stabiler essentieller Hypertonie eine erniedrigte Kallikrein-Ausscheidung vor. Bei Patienten mit labiler essentieller Hypertonie scheint jedoch die Kallikrein-Ausscheidung im Normbereich zu liegen. Diese Befunde lassen vermuten, daß die verschiedentlich bei Patienten mit essentieller Hypertonie festgestellte Erniedrigung der Kallikrein-Ausscheidung eher eine Folge des Hochdrucks als dessen Ursache darstellt. Offenbar spielt das renale Kallikrein-Kinin-System keine primäre Rolle in der Pathogenese der Hypertonie.

[Diurnal profiles of plasma aldosterone, cortisol, renin, angiotensinogen and angiotensinases in normal subjects (author's transl)].

SummaryPlasma cortisol and renin were estimated in 1 h intervals, plasma aldosterone, angiotensinogen and angiotensinases in 3 h intervals over periods of 24 h in six normal volunteers (age 20–26) under control conditions and subsequently under suppression of ACTH released by dexamethasone.Highest cortisol levels were found around 7 a.m., minimum levels between 9 p.m. and 1 a.m. Dexamethasone reduced cortisol to constantly low concentrations.Aldosterone was highest around 4 a.m. under control conditions and under dexamethasone, and showed lowest concentrations between 4 and 10 p.m. There were no significant differences between mean aldosterone concentrations at corresponding time points of the control and the dexamethasone period.Similar to aldosterone, renin showed peak values around 4 a.m. All mean values at corresponding time points between 7 a.m. and 11 p.m. and the 24 hour mean values of each subject were significantly increased under the influence of dexamethasone.No evidence could be achieved for the existence of circadian rhythms of angiotensinogen and angiotensinases. Dexamethasone did not cause significant changes of these parameters.The data suggest that circadian rhythms of aldosterone and renin are similar to each other but not exactly synchronized to that of cortisol. When ACTH release is inhibited by dexamethasone renin increases to maintain normal aldosterone levels. Angiotensinogen and angiotensinases, parameters which may influence the active concentration of angiotensin II, do not seem to be involved in the regulation of aldosterone.ZusammenfassungAn 6 normalen männlichen Freiwilligen im Alter von 20–26 Jahren wurden Plasmacortisol und -renin stündlich, Plasmaaldosteron, -angiotensinogen und -angiotensinasen alle 3 Std über jeweils 24 Std unter Kontrollbedingungen und anschließend unter Suppression der ACTH-Freisetzung durch Dexamethason gemessen.Die höchsten Cortisolspiegel fanden sich gegen 7 Uhr, die niedrigsten zwischen 21 und 1 Uhr. Die Gabe von Dexamethason führte zu konstant niedrigen Cortisolkonzentrationen.Aldosteron war unter Kontrollbedingungen und unter Dexamethason gegen 4 Uhr am höchsten und zeigte niedrigste Werte zwischen 16 und 22 Uhr. Zwischen den mittleren Aldosteronkonzentrationen entsprechender Zeitpunkte der Kontroll- und der Dexamethasonperiode bestanden keine signifikanten Unterschiede.Ähnlich dem Aldosteron zeigte das Plasmarenin Maximalwerte gegen 4 Uhr. Alle Mittelwerte entsprechender Zeitpunkte zwischen 7 und 23 Uhr und die jeweiligen 24 Std-Mittelwerte jedes einzelnen Probanden waren unter dem Einfluß von Dexamethason signifikant erhöht.Für die Existenz circadianer Rhythmen des Angiotensinogens und der Angiotensinasen konnte kein Anhalt gewonnen werden. Dexamethason bewirkte keine signifikanten Veränderungen dieser Parameter.Die Ergebnisse deuten darauf hin, daß die circadianen Rhythmen von Aldosteron und Renin miteinander vergleichbar, jedoch nicht exakt mit dem des Cortisols synchronisiert sind. Unter der Hemmung der ACTH-Freisetzung durch Dexamethason steigt die Reninaktivität an, der Aldosteronspiegel bleibt unverändert. Angiotensinogen und die Angiotensinasen, Parameter, die die aktive Konzentration des Angiotensin II beeinflussen können, scheinen an der Regulation des Aldosterons nicht beteiligt zu sein.Plasma cortisol and renin were estimated in 1 h intervals, plasma aldosterone, angiotensinogen and angiotensinases in 3 h intervals over periods of 24 h in six normal volunteers (age 20-26) under control conditions and subsequently under suppression of ACTH release by dexamethasone. Highest cortisol levels were found around 7 a.m., minimum levels between 9 p.m. and 1 a.m. Dexamethasone reduced cortisol to constantly low concentrations. Aldosterone was highest around 4 a.m. under control conditions and under dexamethasone, and showed lowest concentrations between 4 and 10 p.m. There were no significant differences between mean aldosterone concentrations at corresponding time points of the control and the dexamethasone period. Similar to aldosterone, renen showed peak values around 4 a.m. All mean values at corresponding time points between 7 a.m. and 11 p.m. and the 24 hour mean values of each subject were significantly increased under the influence of dexamethasone. No evidence could be achieved for the existence of circadian rhythms of angiotensinogen and angiotensinases. Dexamethasone did not cause significant changes of these parameters.

Sympathetic nervous activity and the pressor effect of noradrenaline under chronicα-β-adrenoceptor blockade with labetalol in hypertension

SummaryIn 14 patients with essential hypertension, the influence of theα- andβ-adrenoceptor blocking drug labetalol on blood pressure, heart rate, plasma renin, plasma noradrenaline and pressor effect of exogenous noradrenaline was investigated during long-term treatment. During the initial four weeks of treatment, labetalol at a dose of 400 mg/day showed a slight effect only on supine blood pressure, whereas upright blood pressure was already lowered effectively after the second week of treatment (p<0.01). An increase in the mean dose to 850 mg/day had an additional blood pressure-lowering effect (p<0.001), whereby a preferential decrease of the orthostatic blood pressure was no longer apparent. Further increase in the mean dose to 1,000 mg/day at the end of the 12th week did not have an additional blood pressure-lowering effect. Body weight, plasma renin and plasma noradrenaline remained unchanged on labetalol treatment in the lowest and the highest dose. There was, however, an increased pressor effect of exogenous noradrenaline, i.e. anα-adrenoceptor antagonistic effect of labetalol was not detectable under these conditions. The cause of the increased pressor effect was a reduced climination of noradrenaline from plasma, which is probably the consequence of an inhibition of the uptake1 process by labetalol. During long-term treatment with the doses administered, the blood pressure-lowering effect of labetalol appears essentially to be the expression of theβ-adrenoceptor blocking properties of the drug.

Urinary kallikrein in normotensive subjects and in patients with essential hypertension.

1. Excretion of urinary kallikrein was normal in 13 out of 15 patients with uncomplicated essential hypertension. 2. Frusemide increased urinary kallikrein excretion in normotensive subjects and in patients with essential hypertension. The stimulating effect of frusemide on urinary kallikrein was significantly diminished in patients with essential hypertension. 3. No correlations of urinary kallikrein with sodium, potassium, and aldosterone excretion were found. 4. The results do not support the idea that urinary kallikrein plays a primary role in the pathogenesis of essential hypertension.

Low Renin Hypertension

Low renin hypertension probably does not represent a clinical entity. In many patients with low renin hypertension blood pressure is normalized by treatment with diuretics only; in these patients a (genetic?) sensitivity to salt might play a predominant role in the pathogenesis of hypertension and renin suppression. In another group of patients renin suppression appears to be secondary to the hypertensive process. This is indicated by the observation that prevalence of low renin hypertension increases with age and that it is more frequent in advanced stages of hypertension. Also a diminished sympathetic tone might play a part in the renin unresponsiveness. Finally, although no positive evidence was found, the possibility cannot be excluded that, at least in some cases, a mineralocorticoid other than aldosterone is involved. Neither in normotensive subjects nor in hypertensive patients, both with normal and with low plasma renin was a correlation between plasma renin concentration and plasma aldosterone concentration following stimulation by upright posture found. More detailed studies will be necessary to clarify the relationship between the renin-angiotensin system and aldosterone secretion during upright posture, in particular in patients with low renin hypertension.

Kreislaufreaktionen bei Patienten mit primärem Aldosteronismus

Summary1. In 7 patients with hypertension, aldosteronism, and low plasma renin (6 patients with a solitary adrenal adenoma, 1 patient with bilateral adrenal hyperplasia) circulatory reflexes (Valsalvas maneuver, head-up tilt and cold pressure test) were examined. Furthermore, the reactivity to the pressor action of tyramine and norepinephrine was determined. For comparison 10 patients with essential hypertension were studied.2. In 4 of the 7 patients with primary aldosteronism no overshoot following Valsalvas maneuver could be observed. Compared to the patients with essential hypertension the mean overshoot in the patients with primary aldosteronism was significantly reduced. The decrease in blood pressure during head-up tilt was significantly more pronounced in the patients with primary aldosteronism. However, both groups did not differ in their reaction to the cold pressure test. In the patients with primary aldosteronism responsiveness to tyramine was significantly reduced compared to the patients with essential hypertension. No significant difference was observed in the reactivity to norepinephrine between both groups studied.3. The results point towards a disturbance of the sympathetic nervous system in patients with primary aldosteronism.Zusammenfassung1. Bei 7 Patienten mit arterieller Hypertonie, Aldosteronismus und niedrigem Plasmarenin (6 Patienten mit solitärem Nebennierenrindenadenom, 1 Patient mit mikronodulärer Nebennierenrindenhyperplasie) wurden die Kreislaufreaktionen auf den Valsalva-Versuch, auf passive Orthostase und auf den Eiswasserversuch geprüft. Darüber hinaus wurde die Reaktion des Blutdruckes auf Tyramin und Noradrenalin bestimmt. Als Vergleichsgruppe dienten 10 Patienten mit essentieller Hypertonie.2. Bei 4 der 7 Patienten mit primärem Aldosteronismus war kein overshoot nach Valsalva-Versuch nachweisbar. Im Durchschnitt war das Ausmaß des postpressorischen overshoot bei Patienten mit primärem Aldosteronismus signifikant geringer als bei Patienten mit essentieller Hypertonie. Der Abfall des mittleren arteriellen Druckes während der 15 minütigen passiven Orthostase war bei den Patienten mit primärem Aldosteronismus signifikant stärker als bei den Patienten mit essentieller Hypertonie. Ein Unterschied in der Blutdruck reaktion auf den Eiswasserversuch konnte dagegen zwischen beiden Gruppen nicht festgestellt werden. Die pressorische Wirkung von Tyramin war bei den Patienten mit primärem Aldosteronismus im Vergleich zu den Patienten mit essentieller Hypertonie signifikant geringer. In der Empfindlichkeit gegenüber Noradrenalin unterschieden sich beide Gruppen nicht signifikant.3. Die Befunde sprechen für eine nicht näher zu lokalisierende Störung der Sympathikusfunktion bei Patienten mit primärem Aldosteronismus.