Do Resistance Vessel Abnormalities Contribute to the Elevated Blood Pressure of Spontaneously-Hypertensive Rats?

Abstract

This review summarizes some of the evidence pointing to the existence of vascular abnormalities in the spontaneously hypertensive rat (SHR) and the extent to which such abnormalities could be responsible for the elevated blood pressure in this animal. Compared with its genetic normotensive control, the Wistar-Kyoto rat (WKY), the adult SHR has an increased total peripheral resistance (TPR). Many factors appear to contribute to the increased TPR, including an active rarefication of the vascular bed and a general constriction of the vasculature. There is evidence that the general constriction is due to structural differences in the resistance vessels, to abnormally high activation levels (i.e. increased sympathetic nerve activity), and to abnormal excitation-contracting coupling within the vasculature itself (i.e. increased noradrenaline sensitivity of the vascular smooth muscle cells). Age studies and studies of the effects of antihypertensive treatment suggest that both structural and excitation-contraction abnormalities may be present before the onset of hypertension.

Comparison of the effect of endothelin on microvessels and macrovessels in Goldblatt II and deoxycorticosterone acetate-salt hypertensive rats.

“…In the present study, reactivity to endothelin (referred to here as the magnitude of the response as proposed by Murvany 14 ) was increased in the hypertensive state (Gil and DOCA-salt microvessel preparations), whereas a higher sensitivity (used here to describe the facility with which the contractile process in vascular smooth muscle is activated 14 ) was observed in preparations from Gil but not DOCA-salt hypertensive rats.…”

Chronic inhibition of angiotensin converting enzyme decreases Ca2+-dependent tone of aorta in hypertensive rats.

“…This response indicated the absence of endothelial cells. 20 Thereafter, the aortic strip was suspended in an organ bath containing 30 ml KHS maintained at 36.5±0.5° C and aerated with a 5% CO 2 Isometric tension of the aorta was measured with a force-displacement transducer (TB-612T, Nihonkohden, Tokyo, Japan) connected to a carrier amplifier (AP-601G, Nihonkohden). The muscle tension was recorded on a thermal-pen-writing recorder (RJG-4128, Nihonkohden).…”

Different susceptibilities to cerebral infarction in spontaneously hypertensive (SHR) and normotensive Sprague-Dawley rats.

“…Clearly, this susceptibility in SHR and SHRSP was not dissociated in time from the initiation period for hypertension and its associated vascular differences. 30 Morbidity, Premature Death and the Infarct All SHR and SD who became morbid or died received Evans blue by the intraperitoneal route. Premature death did not appear to be secondary to the process of infarction because sham operated rats and rats without infarcts died, yet not one of 5 SHR having an infarct died, even though each received Evans blue intravenously.…”