This study was designed to investigate the possible role of angiotensin and vasopressin in the maintenance of arterial blood pressure during acute blockade of the autonomic nervous system. Two groups of eight dogs each were anesthetized with pentobarbital sodium, and autonomic ganglia were blocked with hexamethonium (20 mg/kg). Thirty minutes later group 1 received the vasopressin antagonist 1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid),2-(O-methyl)tyrosine arginine vasopressin (10 micrograms/kg) followed after a 30-min interval by captopril (1 mg/kg). Group 2 received the same drugs, except the order of administration of vasopressin antagonist and captopril was reversed. Vasopressin antagonist during ganglionic blockade (group 2) produced a greater fall in blood pressure than did captopril during ganglionic blockade (group 1). These data indicate that vasopressin plays a greater pressor role than angiotensin in the acute response to ganglionic blockade. Additional studies were performed to determine if the autonomic nervous system alone can support the resting blood pressure in the anesthetized dog. Combined blockade of angiotensin and vasopressin without autonomic blockade produced a significant decrease in blood pressure, suggesting that the autonomic nervous system alone is not able to support the control blood pressure in the anesthetized dog.

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Vascular responses of the ventral medulla and total brain to 30-60 min of isocapnic hypoxia (PaO2 = 32 +/- 2 Torr) were examined using radioactive microspheres in anesthetized, paralyzed, and artificially ventilated cats. Ventral medullary extracellular fluid (ECF) pH was measured using pH microelectrodes with tip diameters of 1-2 micrometers. Total brain blood flow (Q) increased significantly from a control value of 53 +/- 8 (mean +/- SE) to 160 +/- 42 ml.100 g-1.min-1 following 30-60 min of hypoxia. Ventral medullary Q increased from 28 +/- 5 to 97 +/- 20 ml.100 g-1.min-1 and ECF pH decreased by 0.15 +/- 0.06 pH U. Q responses are attributable to decreased vascular resistance as arterial pressure remained constant. The sensitivity of the ventral medullary vasculature to isocapnic hypoxia did not differ from that of the brain as a whole. The results show that under the conditions of our experiment, the ventral medullary vascular response to hypoxia is not sufficient to stabilize local ECF pH. The observation of simultaneously reduced pH and increased Q is consistent with a role for ECF H+ in mediating the cerebrovascular response to hypoxia.

The ability of two kininase II inhibitors, SQ 20881 and captopril, to inhibit conversion of angiotensin I to angiotensin II and to potentiate the vascular responsiveness to exogenous bradykinin were compared in the mesenteric, renal, and external iliac vasculatures of the dog. Basal rate of angiotensin I-to-angiotensin II conversion was found to be lower in the renal vasculature, average conversion being 4.7%, than in the mesenteric and iliac vasculatures, in which the average conversion was 30.7 and 26.3%, respectively. Inhibition of angiotensin I conversion by both kininase II inhibitors was independent of the basal angiotensin I conversion rate; however, SQ 20881 was a more potent inhibitor of angiotensin I conversion than captopril in all vascular beds tested. In the presence of equal molar doses of SQ 20881 and captopril, only 20-30% of the control bradykinin doses was needed to produce the same vascular effects in the mesenteric and iliac vasculatures. In the kidney, 70% of the control bradykinin doses was needed to produce the same vascular effects in the presence of SQ 20881; in contrast to SQ 20881, neither an equimolar nor 20 times an equimolar dose of captopril produced any change in the renal vascular responsiveness to bradykinin. In conclusion, 1) SQ 20881 is a more potent inhibitor of angiotensin conversion than captopril, and 2) captopril, unlike SQ 20881, does not alter renal vascular responsiveness to bradykinin.

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Adrenal blood flow was measured during hemorrhagic hypotension in pentobarbital-anesthetized dogs using the radioactive-microsphere technique. A decrease in adrenal vascular resistance occurred during hemorrhage that was sufficient to maintain adrenal blood flow at prehemorrhage levels even with a decrease in mean arterial blood pressure (MABP) to as low as 50 mmHG. Blockade of alpha- and beta-adrenergic receptors, H1- and H2-histamine receptors, and prostaglandin synthesis all decreased resting adrenal blood flow. However, blood flow did not decrease further with hemorrhage subsequent to these interventions. Neither cholinergic blockade (muscarinic) alone nor ganglionic blockade subsequent to cholinergic blockade changed adrenal blood flow. However, ganglionic blockade alone increased adrenal blood flow. Hemorrhage subsequent to hypophysectomy also did not change blood flow to the adrenal. These data suggest that the maintenance of adrenal blood flow during hemorrhagic hypotension to 50 mmHg MABP is independent of the autonomic nervous system, prostaglandin synthesis, histamine receptors, or an intact pituitary-adrenal axis, even though all of these systems do influence adrenal blood flow.

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