Hypothalamic responsiveness in DOCA hypertensive rats augmented by streptozotocin-induced diabetes.
In rats with deoxycorticosterone acetate (DOCA) salt hypertension, induction of diabetes with streptozotocin did not aggravate the elevation in blood pressure, but pressor and sympathetic nerve responses to electrical stimulation of the ventromedial hypothalamus were enhanced. Along with glycosuria and hyperglycemia, the other effects of streptozotocin-induced diabetes were: reduced body weight, increased fluid intake, and bradycardia. Despite enhanced responsiveness to hypothalamic stimulation, blood pressure increases produced by intravenous injections of norepinephrine, tyramine, or vasopressin were unaltered. When pressor responses were compared in diabetic rats drinking either tap water or isotonic saline solution, no appreciable differences occurred. It was considered possible that hypothalamic responsiveness was enhanced in diabetic-DOCA hypertensive rats by increases not only in sympathetic nerve firing but also in release of endogenous norepinephrine.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003900:Desoxycorticosterone / Q000633:toxicity*; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D004558:Electric Stimulation; D006339:Heart Rate / Q000187:drug effects; D006943:Hyperglycemia / Q000503:physiopathology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D007031:Hypothalamus / Q000502:physiology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D003900:Desoxycorticosterone