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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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Enhanced activity of renin-angiotensin-aldosterone system has been suggested as a cause of the high blood pressure in certain forms of experimental hypertension. In spontaneously hypertensive rats, however, increased activity of the system has not been found, and even suppressed renin angiotensin system has been reported in the spontaneously hypertensive rat. In the present experiments it was attempted to explore the possible alteration of the short loop negative feedback control in the hypertensive rat. Experiments have been done in the anesthetized spontaneously hypertensive rats(SHR) as well as in normotensive Wistar and Sprague Dawley rats as control. Responses of the plasma renin activity to the intravenous L-isoproterenol were dose dependent, in both SHR and normotensive control rats. Hypotensive responses to smaller do sea of L-isoproterenol were more accentuated in SHR than in the normotensive control rats. Angiotensin If given intravenously suppressed plasma renin activity in a dose dependent fashion in both groups. However, these suppressive responses were significantly attenuated in SHR as compared with the normotensive control rats. Treatment with angiotensin I-converting enzyme inhibitor did not correct the attenuated responses of the plasma renin activity to angiotensin II in SHR. Intravenous infusion of arginine vasopressin also produced a dose-dependent suppression of plasma renin activity in both groups. The responses to arginine vasopressin were also significantly attenuated to the normotensive control rats. In the sodium-depleted SHR, arginine vasopressin did not suppress plasma renin activity, whereas the suppressive responses to arginine vasopressin in the normotensive control rats were not different from the untreated control rats. These data suggest that there may be a derangement in the short loop negative feedback control of the renin-angiotensin system in spontaneously hypertensive rat.
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