title: [Elevation of spontaneous tone and effects of antihypertensive treatments in arterial smooth muscle of spontaneously hypertensive rats].
abstract: Mechanisms of elevation of active tone in arterial smooth muscle of spontaneously hypertensive rats and effects of antihypertensive treatments are reviewed. Spontaneously hypertensive rats are created by Okamoto et al. and classified mainly into three strains, SHR, SHRSP and M-SHRSP. Blood pressure of the rats is higher in this order. The aortic smooth muscle of these rats exhibits elevation of the active tension (tone) under non-stimulated condition. The active tone is greater as the blood pressure of the rats elevated and good correlation between blood pressure and active tone can be obtained. The active tone is sensitive to extracellular Ca and abolished by the removal of extracellular Ca or by the application of Ca-antagonists. It is also associated with increased intracellular Ca level. These results indicate that the active tone is brought about by increase in voltage-dependent Ca channel opening of the cell membrane. Increased voltage-dependent Ca channel opening, i.e. membrane depolarization and increased inward Ca current can be a cause of the elevated tone. Abnormalities in the cellular mechanisms for relaxation of the smooth muscle can also contribute to the elevation of the active tone. Endothelium suppresses the active tone, probably releasing endothelium-derived relaxing factor or hyperpolarizing factor. The suppression of contraction by endothelium is impaired in the blood vessels of spontaneously hypertensive rats, depending on the degree of hypertension. Antihypertensive treatments prevent the development or elevation of the active tone. It also prevents the impairment of function of endothelium. Thus, the maintained hypertension alters functions of smooth muscle membrane and endothelium. The degree and duration of hypertension are thought to be determinant factors of these abnormalities.
authors.affiliation: Research Institute of Hypertension, Kinki University, Osaka.
authors.forename: S
authors.initials: S
authors.lastname: Sunano
authors.forename: F
authors.initials: F
authors.lastname: Sasaki
mesh_terms: D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001158:Arteries / Q000187:drug effects; D001794:Blood Pressure; D002118:Calcium / Q000502:physiology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000502:physiology; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology; D051381:Rats; D011918:Rats, Inbred SHR
chemical_list: D000959:Antihypertensive Agents; D009569:Nitric Oxide; D002118:Calcium