Kuniaki Matsui

Role of intracerebral angiotensin receptors in the regulation of vasopressin release and the cardiovascular system.

In order to investigate the physiological role of the brain renin-angiotensin system in the regulation of vasopressin (ADH) release, angiotensin II (Ang II, 10 ng/kg/min) or 1-Sar-8-Ile-Ang II (50 ng/kg/min), an Ang II antagonist, was administered intracerebroventricularly to dogs (n = 42) anesthetized with urethane and chloralose after morphine sedation. The effects of the intravenous infusion of either 0.15 M or 2.5 M NaCl (0.1 ml/kg/min, 75 min) were also studied. In control dogs, artificial cerebrospinal fluid (ACSF) was administered at a rate of 10 microliter/min for 105 min. ACSF given intracerebroventricularly plus 0.15 M NaCl given intravenously did not affect ADH release, but 2.5 M NaCl given intravenously raised the plasma ADH level in parallel with the rise in plasma osmolality. Heart rate and blood pressure did not change significantly in ACSF along with 0.15 M NaCl, but heart rate increased significantly in ACSF along with 2.5 M NaCl. Ang II along with 0.15 M NaCl significantly raised plasma ADH and decreased heart rate without any changes in blood pressure. Ang II along with 2.5 M NaCl brought about a significant rise in plasma ADH level, arterial blood pressure, heart rate, and plasma osmolality. But simultaneous application of Ang II and 2.5 M NaCl did not result in a larger rise in plasma ADH than that expected from the effects of the two stimulations given separately. Namely, Ang II did not potentiate ADH release elicited by osmotic stimulation. Ang II antagonist given intracerebroventricularly neither affected ADH release and the cardiovascular system in 0.15 M NaCl nor inhibited ADH release in response to osmotic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Hemorrhagic Shock on Plasma Met-enkephalin, Vasopressin, Catecholamines, and Cardiovascular Functions in Intact and Adrenalectomized Dogs

It is well known that enkephalins in the brain, unlike the adrenal gland and sympathetic nervous system, coexist with vasopressinergic neurons in the hypothalamoneuro- hypophyseal system (Martin and Voigt 1981; Martin et al. 1983). Moreover, the enkephalin contents of this region have been reported to decrease in dehydrated rats and/or Brattleboro rats with a genetic defect in vasopressin synthesis (Marina et al. 1977; Rossier et al. 1979). Furthermore, it has recently been documented that plasma enkephalin-like immunoreactivity is increased in animals with endotoxic or hemorrhagic shock (Evans et al. 1984; Lang et al. 1982), reminiscent of vasopressin release in hypotensive shock (Share 1974).

A case of central diabetes insipidus associated with pituitary apoplexy

症例は56才の男.主訴は頭痛と悪心.昭和51年頃より性欲低下その後易疲労感を覚えるようになつた.昭和55年3月13日,突然悪心,頭痛出現,某医にて血性髄液所見より,くも膜下出血を疑われ脳卒中センターに入院する.その後,頭部X線写真上トルコ鞍のballooningが認められたためpituitary apoplexyと診断される.前医入院時意識は清明で血清Na値は130mEq/lであつたが,第7病日に105mEq/lに低下し呼吸停止等の水中毒症状を呈した.しかし,水制限により低Na血症は改善したため,内分泌学的検査のため当科へ転入院した.血中T3, T4値はそれぞれ112ng/d1, 11.3μg/dlと正常であり,血中コルチゾールは1.6μg/dl,尿中17OHCS, KS値はそれぞれ1.1, 1.5mg/日と低値であつた. glucocorticoidを補充したところ尿量が7～12l/日と急増し,尿崩症の存在が考えられた.脱水試験では血漿漫透圧が289mOsm/kgと高値にもかかわらず,尿浸透圧は84mOsm/kgと低値で,バゾプレシン投与後は484mOsm/kgまで上昇した.血中および尿中ADH値も0.8pg/ml, 1.6ng/hと低値で,中枢性尿崩症と診断した. DDAVP10μg/日補充後尿量は2l/日以下となり,下垂体腫瘍摘出術を行なつたが,腫瘍組織は特定できなかつた. pituitary apoplexyに永続的尿崩症を合併することは極めてまれで報告例は少ない.尿崩症の発生機序は不明であるが,出血後の血管攣縮等により視床下部付近にまで障害が及んだためと考えられた.