PT  - JOURNAL ARTICLE
AU  - J Q Kong
AU  - D A Taylor
AU  - W W Fleming
TI  - Mesenteric vascular responses of young spontaneously hypertensive rats.
DP  - 1991 Jul 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 13--17
VI  - 258
IP  - 1
4099  - http://jpet.aspetjournals.org/content/258/1/13.short
4100  - http://jpet.aspetjournals.org/content/258/1/13.full
SO  - J Pharmacol Exp Ther1991 Jul 01; 258
AB  - Frequency-responses curves for nerve stimulation and dose-response curve for norepinephrine, 5-hydroxytryptamine potassium chloride, vasopressin and acetylcholine (ACh) were determined in isolated, perfused mesenteric vascular beds from young (approximately 5 weeks) spontanelouly hypertensive (SHR) and Wistar Kyoto rats. Although mean systolic blood pressure (measured by tail cuff plethysmography) was slightly higher in the SHR, this difference was not significant. Slopes and maximum responses were increased significantly for nerve stimulation and all agonists. The basal perfusion pressure was also significantly elevated in the SHR. These differences are consistent with existing evidence that structural changes occur in blood vessels of SHR at an early stage and probably precede development of hypertension. Such structural changes could therefore contribute to development of the hypertension. Cocaine (1 microM) markedly increased responses to nerve stimulation and bolus injections of norepinephrine in preparations from SHR with little or no effect on such responses in Wistar Kyoto preparations, a result consistent with the known greater density of noradrenergic nerves in SHR vasculature. In the presence of cocaine, there was unmasked a selective super-sensitivity (significantly lower ED50) to norepinephrine in the SHR. Thus SHR mesenteric vessels may possess an alteration in adrenoreceptors or their coupling to other cellular mechanisms. Responses to ACh revealed no indication of a deficient endothelial mediated relaxation. An altered media:lumen ratio of small arteries, hypernoradrenergic innervation and supersensitivity to the transmitter may contribute to development of hypertension.