Why the study?
Does intracerebroventricular angiotensin II injection alter physiological responses in spontaneously hypertensive rats compared to normotensive controls?
Does intracerebroventricular angiotensin II injection alter physiological responses in spontaneously hypertensive rats compared to normotensive controls?
The brain isorenin-angiotensin system may contribute to spontaneous hypertension via increased angiotensin II production or potentiated sympathetic activation, rather than generalized increased central receptor sensitivity.
Rat data indicate selective central angiotensin II effects without clinical translation; leaves open targeted brain RAS roles in hypertension.
The brain isorenin angiotensin system has been implicated in the development of spontaneous hypertension by several investigators. The experiments reported here were designed to test the responsiveness of unanesthetized spontaneous hypertensive (SH) rats to intracerebroventricular angiotensin II injections compared to Wistar-Kyoto (WK) normotensive controls. The results indicate that there is no difference between SH and WK animals in drinking responses or antidiuretic hormone release to central angiotensin II injections; however, an increased pressor responsiveness to intraventricular angiotensin II in SH as compared to WK was observed. The results of intravenous infusions of pressor substances in these experiments and reports by other investigators suggest that the increased blood pressure effects to central angiotensin are due to three possible factors: 1) increased vascular responsiveness of SH to vasoconstrictor substances in general, 2) increased vascular sensitivity of SH rats to sympathetic outflow, and 3) decreased baroreceptor reflexes to acute increases in blood pressure. We suggest that the brain isorenin-angiotensin system may be involved in spontaneous hypertension by increased production of angiotensin II or by activation of a potentiated sympathetic system, but not by a generalized increased sensitivity of brain receptors to central angiotensin.
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Hoffman et al. (1977) studied this question.
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