-transparent.png){kind=logo}
Vascular angiotensin converting enzyme could contribute to the elevated vascular resistance found in hypertension. The purpose of this study was to determine if angiotensin converting enzyme activity was present in the hindquarter vasculature of one model of hypertension, the spontaneously hypertensive rat (SHR) and its normotensive control, the Wistar-Kyoto rat (WKY). We evaluated the effect of a maximal blocking dose of captopril (0.5 mg) on the angiotensin I pressor response during the infusion of the hindquarter with an artificial perfusate. Angiotensin I (1000 ng/ml) produced a significant increase in peripheral vascular resistance (PVR) in both SHR and WKY, but the increase was greater in SHR. Captopril inhibited the elevation in PVR in both. A lower concentration of angiotensin I (250 ng/ml) produced a significant and similar pressor response in SHR (less than the pressor response to 1000 ng/ml) and WKY (same as the pressor response to 1000 ng/ml). Again, captopril prevented the elevation in PVR to A1 in both SHR and WKY. Because these studies were performed using an artificial perfusate, angiotensin converting enzyme must be present in the SHR and WKY hindquarter vasculature including resistance vessels.
S M Mueller, and
M L Cohen
December 1982,
Neuroscience letters,
S M Mueller, and
M L Cohen
October 1979,
Nihon rinsho. Japanese journal of clinical medicine,
S M Mueller, and
M L Cohen
February 1990,
Circulation research,
S M Mueller, and
M L Cohen
February 1996,
Clinical and experimental hypertension (New York, N.Y. : 1993),
S M Mueller, and
M L Cohen
March 1988,
Brain research,
S M Mueller, and
M L Cohen
January 1987,
Journal of the American Veterinary Medical Association,
S M Mueller, and
M L Cohen
March 1984,
Rational drug therapy,
S M Mueller, and
M L Cohen
January 1985,
Clinical science (London, England : 1979),
S M Mueller, and
M L Cohen
December 2003,
Journal of applied physiology (Bethesda, Md. : 1985),
S M Mueller, and
M L Cohen
September 1998,
FEBS letters,
