Vasoconstriction and Hypersensitivity to Vasoactive Substances After Acute Volume Expansion in Dogs

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 1988-07, Vol.12 (1), p.59-66
• Main Authors: OTSUKA, ATSUHIRO, OGIHARA, TOSHIO, KOHÁRA, KATSUHIKO, MLKAMI, HOROSHI, KATAHIRA, KATSUTOSHI, TSUNETOSHI, TAKESHI, KUMAHARA, YUICHI
• Format: Article
• Language: English
• Subjects: Aldosterone - blood; Angiotensin II - pharmacology; Animals; Atrial Natriuretic Factor - blood; Blood Volume - drug effects; Cardiac Output - drug effects; Dextrans - pharmacology; Dogs; Epinephrine - blood; Epinephrine - pharmacology; Heart Rate - drug effects; Hypertension - etiology; Natriuresis - drug effects; Norepinephrine - blood; Renin - blood; Vascular Resistance - drug effects; Vasoconstriction - drug effects; Vasopressins - blood
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.HYP.12.1.59

In a search for factors contributing to the sustained Mood pressure (BP) elevation in acutely volume-loaded animals, dextran dissolved in lactated Ringerʼs solution (20 ml/kg) was infused into 34 mongrel dogs over a period of 1 hour under pentobarbital anesthesia and changes in bemodynamic and humoral variables were monitored during its infusion and for 3 hours after its infusion. BP elevation during volume loading (from 114 ± 3 to 128 ± 3 [SEM] mm Hg) was attributed to an increase in cardiac output. After volume loading, some dogs maintained BP elevation whereas others did not. The former group showed an increase in total peripheral resistance, demonstrating a transformation of cardiac output to total peripheral resistance as a responsible factor in maintenance of the elevated BP. The plasma levels of norepinephrine, vasopressin, and plasma renin activity were not elevated, indicating that these vasoactive factors were not responsible for elevation of the BP or total peripheral resistance. The changes in the hematocrit, atrial natriuretk factor, urine volume, and urinary sodium excretion were identical in the two groups, and natrluresis was not prominent when total peripheral resistance was high. Pressor responses to norepinephrine and angiotensin II were potentiated 3 hours after stopping Infusion in both groups, but this potentiation was not correlated with the Increase in total peripheral resistance or mean BP. Thus, acute volume expansion produced resistance-dependent hypertension following the initial volume-dependent hypertension. It is unlikely that a vascular sensitizing natriuretk factor plays a role in the resistance-dependent BP elevation. The mechanism and physiological importance of hypersensitivity to vasoactive substances remain to be elucidated.