Abstract
The spontaneously hypertensive rat (SHR) is a commonly used animal model of hypertension and transplantation studies provide evidence for a renal element to the aetiology of the hypertensive process. This study was designed to test the hypothesis that the contractile function of the ureter of the SHR differs to that of the normotensive control Wistar-Kyoto (WKY) rat. Ureter segments from SHR (n = 16) and WKY (n = 16) were cannulated and pressurised in vitro. Acetylcholine (ACh) was used to stimulate phasic contractile pressure responses. SHR ureter contractile frequencies were significantly greater than those of WKY (6.6 ± 0.8 vs. 3.8 ± 0.2 min(-1) in 10(-5) M ACh; p < 0.01). Magnitudes of contractile responses were not significantly different (SHR 14.3 ± 1.5 mmHg, WKY 15.2 ± 2.1 mmHg). SHR ureteral contractile function differs significantly to that of normotensive WKY. Ureteral dysfunction may be a contributory causative factor in the aetiology of the hypertensive disease process.
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