AJP - Heart and Circulatory Physiology, Vol 265, Issue 6 2027-H2035, Copyright © 1993 by American Physiological Society

ARTICLES

Vasopressin and oxytocin: modulators of neurohypophysial blood flow

P. D. Hurn, D. A. Wilson, R. B. Hansen, D. F. Hanley and R. J. Traystman
Department of Anesthesiology/Critical Care Medicine and Neurology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287.

We examined the role of arginine vasopressin (AVP) as a mediator of neurohypophysial (NH) blood flow regulation in anesthetized dogs. First, we evaluated the NH hyperemia that occurs during hemorrhagic hypotension in the presence (n = 7) and absence (n = 7) of the selective AVP-V1 receptor antagonist [d(CH2)5Tyr(Me)]AVP. AVP-V1 blockade did not alter NH transient or steady-state flow responses to a standardized decrease to 80 mmHg mean arterial blood pressure. We then determined whether exogenous AVP alters NH and regional cerebral blood flow (CBF) (n = 8). Sequential intracarotid infusions resulted in sagittal sinus blood AVP concentrations ranging from 6.97 +/- 3.3 x 10(3) to 2.45 +/- 0.47 x 10(6) pg/ml. No change in NH blood flow (control 428 +/- 162 vs. 487 +/- 75 ml.min-1.100 g-1) was observed even at the highest blood level. However, CBF at the highest AVP level increased from a control value of 20 +/- 3 to 40 +/- 4 ml.min-1.100 g-1, while cerebral oxygen consumption remained unchanged. Administration of a selective AVP-V1 receptor antagonist, [d(CH2)5Tyr(Me)]AVP, blocked AVP-induced elevation in CBF in a third set of dogs (n = 5). Oxytocin was also given by intracarotid infusion at a constant rate (1-200 micrograms/ml) in a final group (n = 5). NH blood flow was unchanged at all doses, whereas CBF increased from control (24 +/- 2 to 38 +/- 5 ml.min-1.100 g-1) at the highest dose. (ABSTRACT TRUNCATED AT 250 WORDS)

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