Abstract
Changes in vascular smooth muscle tone in hypertension — Development of essential hypertension in man and in the genetically altered spontaneously hypertensive rat (SHR) model of this disease is characterized hemodynamically by a transient elevation in cardiac output, a sustained elevation in total peripheral resistance (TPR) and a reduction in venous capacitance (1,2). The results of many investigations indicate that, in addition to pressure mediated structural adaptation on the arterial side of the circulation (3,4), an increased vascular smooth muscle (VSM) tone contributes significantly to the latter two hemodynamic changes. In the SHR model this increase in VSM tone includes an elevated sympathetic efferent input (5,6) which may be the result of an alteration in a central nervous sensing system (7). In addition, defects in the SHR VSM cell membrane mechanisms that regulate intracellular “activator calcium” (Cai) and therefore excitation-contraction coupling have been postulated to explain observed elevated sensitivity to external neurogenic and humoral influences in certain vessels (7,8,9,10). The defects in these membrane regulatory mechanisms and their temporal relation to the development and maintenance of the elevated VSM tone in SHR remain to be established, particularly in the small resistance and capacitance vessels. In addition to transmembrane ionic flux measurements (11,12), two other important parameters that can be used to assess changes in these membrane regulatory mechanisms are the VSM transmembrane potential (Em)(6,13,14) and the contractile force (7,8,9).
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© 1984 Martinus Nijhoff Publishing, Boston
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Stekiel, W.J., Burke, M.J., Contney, S.J., Lombard, J.H. (1984). In Situ Small Blood Vessel Electrical Response to Verapamil in Spontaneously Hypertensive Rats. In: Sperelakis, N., Caulfield, J.B. (eds) Calcium Antagonists. Developments in Cardiovascular Medicine, vol 39. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-3810-9_20
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DOI: https://doi.org/10.1007/978-1-4613-3810-9_20
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