A study of the relationship between the chemical sensitivity of smooth muscle and the blood pressure of genetically hypertensive rats

An increased neuronal uptake and postsynaptic sensitivity to noradrenaline in arterial smooth muscle from spontaneously hypertensive rats (SHR) has been reported by numerous laboratories. Also reported are changes in vascular reactivity of perfused arterial beds, and a deficiency in homeostasis of intracellular calcium (Ca²⁺) in some tissues of SHR. The work presented here studied these changes in SHR and related animals to determine their relationship to the blood pressure. Also, these changes were studied in another model of genetic hypertension, the Dahl model of salt-sensitive (DS) hypertensive and salt-resistant (DR) normotensive rats. -- Increased neuronal uptake of noradrenaline in arterial smooth muscle (tail artery) was present from 6-8 week onward in SHR related animals. This became more pronounced at the later age groups studies (12-16 week and > 52 week old). In venous (portal vein) and non-vascular (anococcygeus) smooth muscle increased neural uptake of noradrenaline was present in only the very old SHR-related animals. Postsynaptic sensitivity to noradrenaline was increased only in tail arteries from very old SHR. The increased uptake 1 and enhanced postsynaptic sensitivity to noradrenaline were not present in DS and DR rats; in fact there was a trend for reduced uptake 1 activity in tissues from the DS hypertensive rat. -- While perfused mesenteric beds isolated from 12-16 week SHR had a greater reactivity and contractility to noradrenaline, no such changes were observed in mesenteric beds from DS and DR using either noradrenaline, phenylephrine or serotonin as the agonist. The results using papaverine-induced relaxations of DS and DR aortae also suggested no aberrations in sequestration of Ca²⁺ in the Dahl rat. -- The response to La³⁺, thought to reflect a more mobile pool of Ca²⁺ in the SHR, correlated with blood pressure in SHR-related animals when the results were expressed as a percentage of the maximal noradrenaline response, but was not correlated when expressed as mg tension per mg tissue weight. This was due to a negative correlation between blood pressure and the maximal response to noradrenaline in these animals. -- The results reported in this study suggested that alterations in pharmacological and mechanical properties of vascular smooth muscle observed in SHR were probably unique to that model of genetic hypertension