Reactivity of vasa deferentia from spontaneously hypertensive and normotensive Wistar rats.

Abstract

Vasa deferentia from age-matched spontaneously hypertensive rats (SHR) compared with three strains of control rats were found to be hyperresponsive to low concentrations, 10 and 20 mM, of KCl (K+) but not to noradrenaline (NA); the SHR tissue also demonstrated a lower ED50 to K+. Significant differences in maximum tension between SHR and the control animals in response to K+ were not seen although maximum tension developed to K+ was always greater than that developed to NA in either SHR or a control group. The loss of contractile response to K+ in the absence of extracellular calcium was more rapid in the SHR than in the control animals but no such difference was noted for the loss of response to NA. Differences in the Ca2+ dependence of KCl responses were found for 15- to 17-week-old SHR but not for 5- to 7-week-old SHR while differences in the Ca2+ dependence of the NA response were noted in the younger age group of SHR but were less evident compared with the K+ response in the older age group of rat. The 15- to 17-week-old SHR, but not 5- to 7- or 9- to 11-week groups, also demonstrated a hypersensitivity to Ba2+ whereas both SHR and normotensive control tissues demonstrated an extracellular Ca2+-independent and D 600 insensitive contractile response to lanthanum (La3+). The contractile response of the vas deferens to La3+ could, in part, be related to an effect of raised H+ but a pH-independent action of La3+ was also evident from studies with Tris-buffered solutions. Although the action of La3+ was similar in both SHR and control rats the SHR tissue was shown to be more sensitive to H+. The results demonstrate an altered threshold sensitivity and altered responsiveness of nonvascular smooth muscle in the SHR which parallels, in some respects, previous studies indicating altered vascular smooth muscle responsiveness to a variety of physiological and nonphysiological stimuli in the SHR. Furthermore, these studies may indicate that a generalized genetic alteration in the sensitivity of the smooth muscle cell to chemical stimulation and Ca2+ utilization may persist in the SHR. Whether such differences relate to the elevated blood pressure and etiology of hypertension is not yet clear.