Force–velocity relationships in hypertensive arterial smooth muscle

Publisher Website
Google Scholar
Abstract
Increased total peripheral resistance is the cardinal haemodynamic disorder in essential hypertension. This could be secondary to alterations in the mechanical properties of vascular smooth muscle. Adequate study has not been made of the force–velocity (F–V) relationship in hypertensive arterial smooth muscle. Increased shortening in arterial smooth muscle would result in greater narrowing of arteries. The objectives of this investigation were to see if there is (i) increased shortening or increased maximum change in muscle length (ΔLmax where L stands for muscle length), (ii) an increased maximum velocity of shortening (Vmax) measured in lo per second where lo is the optimal muscle length for tension development, and (iii) a difference in maximum isometric tension (Po) developed in spontaneously hypertensive rat (SHR; N = 6) compared with normotensive Wistar Kyoto rat (WKY; N = 5) caudal artery strips. An electromagnetic muscle lever was employed in recording force–velocity data. Analysis of these data revealed the following: (a) the SHR mean Po of 6.21 ± 1.01 N/cm2 was not different from the mean WKY Po of 6.97 ± 1.64 N/cm2 (p > 0.05); (b) the SHR preparations showed greater shortening for all loads imposed; (c) the SHR Vmax of 0.016 lo/s was greater than the WKY Vmax of 0.013 lo/s (p < 0.05). This study provides evidence that while hypertensive arterial smooth muscle is not able to produce more force than normotensive arterial smooth muscle, it is capable of faster and greater shortening. The latter could result in increased narrowing of hypertensive arteries and increased blood pressure.