Peripheral pressor effects of sympathetic stimulation, noradrenaline, angiotensin II and vasopressin in Brattleboro rats.
The following study was designed to test the hypothesis that peripheral blood vessels of vasopressin deficient (Di/Di) rats are less responsive to pressor substances than normal rats. To address this question, pithed Di/Di and normal Long-Evans rats (LE) were exposed to intravenous injections of arginine-vasopressin, angiotensin II and noradrenaline. In addition, blood pressure increments and noradrenaline release in response to spinal cord stimulation in pithed Di/Di and LE rats were studied. The results show no abnormalities in peripheral vascular sensitivity to any of the pressor substances administered, nor was there any change in blood pressure and sympatho-adrenomedullary response to graded stimulation of the sympathetic outflow from the spinal cord. This study suggests that the failure of vasopressin deficient rats to recover from acute hemorrhage is not due to hyporesponsiveness of the peripheral vasculature to pressor agents but, rather, to the deficiency in the direct pressor effect of vasopressin.
D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D001127:Arginine Vasopressin / Q000502:physiology*; D001794:Blood Pressure; D004558:Electric Stimulation; D004837:Epinephrine / Q000097:blood; D006339:Heart Rate; D009638:Norepinephrine / Q000097:blood / Q000502:physiology*; D051381:Rats; D011910:Rats, Brattleboro; D013116:Spinal Cord / Q000502:physiology
D000804:Angiotensin II; D001127:Arginine Vasopressin; D009638:Norepinephrine; D004837:Epinephrine