Role of spinal V1a receptors in regulation of arterial pressure during acute and chronic osmotic stress.
Vasopressinergic neurons in the paraventricular nucleus project to areas in the spinal cord from which sympathetic nerves originate. This pathway is hypothesized to be involved in the regulation of mean arterial pressure (MAP), particularly under various conditions of osmotic stress. Several studies measuring sympathetic nerve activity support this hypothesis. However, the evidence that spinal vasopressin influences MAP under physiological or pathophysiological conditions in conscious animals is limited. The purpose of this study was to investigate, in conscious rats, if the increases in MAP during acute or chronic osmotic stimuli are due to activation of spinal vasopressin (V1a) receptors. Three conditions of osmotic stress were examined: acute intravenous hypertonic saline, 24- and 48-h water deprivation, and 4 wk of DOCA-salt treatment. Rats were chronically instrumented with an indwelling catheter for intrathecal injections and a radiotelemeter to measure MAP. In normotensive rats, intrathecal vasopressin and V1a agonist increased MAP, heart rate, and motor activity; these responses were blocked by pretreatment with an intrathecal V1a receptor antagonist. However, when the intrathecal V1a antagonist was given during the three conditions of osmotic stress to investigate the role of "endogenous" vasopressin, the antagonist had no effect on MAP, heart rate, or motor activity. Contrary to the hypothesis suggested by previous studies, these findings indicate that spinal V1a receptors are not required for elevations of MAP under conditions of acute or chronic osmotic stress in conscious rats.
Dept. of Integrative Biology and Physiology, University of Minnesota, 6-125 Jackson Hall, 321 Church St. S.E., Minneapolis, MN 55455, USA.
Britta
B
Veitenheimer
John W
JW
Osborn
D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D003900:Desoxycorticosterone / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D007278:Injections, Spinal; D008297:Male; D009951:Ornipressin / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000494:pharmacology; D009997:Osmotic Pressure / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017483:Receptors, Vasopressin / Q000819:agonists / Q000502:physiology*; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage / Q000494:pharmacology; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology*; D013312:Stress, Physiological / Q000502:physiology*; D014868:Water Deprivation / Q000502:physiology
D065092:Antidiuretic Hormone Receptor Antagonists; D017483:Receptors, Vasopressin; D012462:Saline Solution, Hypertonic; C082351:vasopressin, Phe(2)-Ile(3)-Orn(8)-; C509323:vasopressin, d(CH2)5(1)-Tyr(OMe)(2)-Arg(8)-; D001127:Arginine Vasopressin; D009951:Ornipressin; D003900:Desoxycorticosterone