Patricia A. Klase

Urethane Anesthesia in Rats

Anesthesia in rats produced by urethane administered intraperitoneally caused (1) peritoneal fluid accumulation; (2) inability to undergo a renal response to NaCl or water loading, and (3) pronounced

Role of calcium ions in the stimulatory actions of luteinizing hormone in isolated ovarian cells: Studies with divalent-cation ionophores

Abstract The divalent-cation ionophores A23187 and ionomycin exert dose-dependent suppressive effects on the stimulatory actions of luteinizing hormone in ovarian cells in vitro . Micromolar concentrations of both A23187 and ionomycin can inhibit the production of progesterone and the stimulation of ornithine decarboxylase activity. Inhibitory concentrations of these ionophores deplete total cell content of calcium, and also seem to suppress protein synthesis.

Centrally Mediated Hydration Effects of Angiotensin in Various States of Sodium Balance

Angiotensin, present in the central nervous system and kidneys, affects salt/water balance when administered to either site but the relationship between central and peripheral actions is unclear. One reported difference between central and peripheral administration of the peptide is that the former causes natriuresis whereas the latter conserves sodium. We injected angiotensin II into the lateral cerebroventricles of conscious rats maintained on low, normal and high sodium intakes. Prior to injection, plasma [Na+] and hematocrits were similar in the 3 groups. Angiotensin increased plasma vasopressin content in all groups at 1 and 5 min; the 1-min peak was greater in the high Na+ rats. In control and low Na+ rats plasma renin activity (PRA) was suppressed 5 and 20 min after angiotensin. Basal PRA of high Na+ rats was low and tended to be further suppressed by angiotensin. Angiotensin-induced water intake was similar in all groups. Thus, the response pattern to intraventricular angiotensin (vasopressin release, PRA suppression and drinking behavior) occurred over a range of sodium intakes sufficient to suppress or elevate basal PRA. These responses, and the natriuretic effect of intraventricular angiotensin, would be beneficial under conditions of Na+ excess. Conversely, these effects would be detrimental in Na+-deficient conditions since they reduce the ability to maintain extracellular [Na+]. Angiotensin effects in brain may be increased by sodium excess whereas the renal angiotensin system is utilized in response to Na+ deficiency.

Consummatory behavior and urine production after cerebroventricular injection of vasopressin and vasopressin antiserum

Vasopressin, or vasopressin antiserum, was injected into a lateral cerebral ventricle of conscious rats. These rats were normally hydrated, cellular dehydrated (NaCl loading) or hypovolemic (polyethylene glycol model). Elevation or reduction of vasopressin in cerebrospinal fluid produced no consistent change in consummatory behavior, urine volume or sodium and potassium excretion. These results show vasopressin in cerebrospinal fluid not to be an absolute requirement for maintenance of hydration or for response to acute volume and osmotic stimuli.

On the Role of Angiotensin in the Cerebellum

Summary Deep cerebellar nuclei contain angiotensin-positive synapses and high affinity receptors for angiotensin have been found in the cerebellum. Four known central effects of angiotensin were examined after injection of the peptide into the region of the dentate-interpositus nuclei: blood pressure elevation, drinking behavior, vasopressin release and ACTH release. None of these effects could be demonstrated, although the dose of angiotensin was known to produce effects when injected at other sites. The results suggest that angiotensin actions in this cerebellar region may be distinct from its known cardiovascular and hydration effects.

Drinking in water deprived rats after combined central angiotensin receptor and converting enzyme blockade

Saralasin, an angiotensin II receptor antagonist, is ineffective in reducing drinking after water-deprivation (WD). Angiotensin III has considerable dipsogenic potency. It may be formed without angiotensin II as an intermediate. To clarify whether angiotensin III formation masks a role for angiotensin in WD, 48 hr WD rats were infused via a lateral cerebroventricle with a) CSF, b) Saralasin, c) SQ 20,881, a converting enzyme inhibitor, or d) Saralasin + SQ. No drug effect on drinking was observed. The results demonstrate that angiotensin III is not required for WD drinking.

Drinking Behavior in Water Deprived Rats after Angiotensin Receptor Blockade

Angiotensin II is a peptide normally present in the bloodstream and central nervous system. Exogenous angiotensin induces drinking which is inhibited by saralasin, a specific receptor antagonist. Administration of saralasin does not reduce endogenously stimulated drinking. Angiotensin is dipsogenic after intravenous or intracerebroventricular infusion, raising the possibility of multiple access routes to the brain. Water deprived rats were given saralasin by both routes simultaneously to block the access of endogenous angiotensin to recentors reached from blood and ventricular cerebrospinal fluid (CSF). Water deprivation increased plasma (Na+), hematocrit, vasopressin content and renin activity but saralasin treatment did not reduce water intake after 30 or 60 min. Therefore, blood or CSF-bore angiotensin does not appear to be an absolute requirement for water deprivation drinking behavior.