Effect of stress on the control of renin release in spontaneously hypertensive rats.
Recent reports suggest that centrally induced increases in sympathetic outflow to the kidney have the potential to enhance the sensitivity of pressure-dependent renin release. In the present study, the possibility was investigated that spontaneously hypertensive rats (SHR), which are thought to have increased tonic sympathetic outflow to the kidney, exhibit enhanced renin release in response to reduced renal perfusion pressure. The increase in plasma renin activity in response to a graded suprarenal aortic constriction was determined in conscious young (6-9 weeks of age) and adult (14-16 weeks of age) SHR and age-matched Wistar-Kyoto (WKY) control rats. Under conditions of relatively little stress, the renin response to reduced renal perfusion pressure was not enhanced in young or adult SHR when compared with age-matched WKY rats. That is, this regulatory mechanism was not "reset" in the hypertensive animals. When challenged with an acute stress (air to the face) both age groups of SHR exhibited a significantly enhanced response. Neither age group of WKY rats was affected by the acute air stress. These data suggest that, under unstressed conditions, pressure-dependent renin release probably does not contribute to the elevation of arterial pressure in the SHR. However, under stressful conditions, the contribution of this system may be significant. Intermittent increases in sympathetic outflow to the kidney that can occur in the SHR in response to daily stresses have the potential to render it more sensitive to spontaneous reductions in perfusion pressure. Occasional exaggerated release of renin could then contribute to the hypertensive process.
- Copyright © 1990 by American Heart Association