Tension–velocity relationships in hypertensive mesenteric resistance arteries

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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 tension–velocity (T–V) relationship in hypertensive resistance arterial smooth muscle. Increased narrowing in such arteries would result in increased resistance. The objectives of this investigation were to determine whether there is (i) increased narrowing capacity (−ΔC/Co where C stands for arterial internal circumference and Co is the optimal arterial internal circumference for maximum tension development); (ii) an increased maximum velocity of isobaric narrowing (Vmax) measured in Co per second; (iii) an increased wall thickness (h); and (iv) an increased active stress development (Tmax) in the spontaneously hypertensive rat (SHR; n = 5) compared with the normotensive Wistar Kyoto (WKY; n = 5) and MK-421 (an angiotensin I converting enzyme inhibitor) treated spontaneously hypertensive rat (MK-421 trt. SHR; n = 5) mesenteric resistance (diameter, < 300 μm) arteries. Analysis of the data for arteries constricting isobarically against a range of pressures revealed that (a) the SHR–ΔC/Co values at pressures ranging from 20 to 120 mmHg (1 mmHg = 133.322 Pa) showed significantly increased narrowing compared with the MK-421 trt. SHR and WKY–ΔC/Co values in this same pressure range (p < 0.01), and (b) the SHR derived Vmax of 0.83 ± 0.08 Co/s was significantly faster than either the MK-421 trt. SHR or WKY Vmax of 0.34 ± 0.06 and 0.28 ± 0.08 Co/s, respectively (p < 0.01); (c) the SHR mean h of 31 ± 3 μm was significantly thicker than either the MK-421 trt. SHR or WKY arteries of 22 ± 2 and 19.5 ± 0.5μm, respectively (p < 0.05); (d) the SHR, MK-421 trt. SHR, and WKY arteries showed no differences in Tmax which were 1016 ± 135, 897 ± 221, and 1077 ± 43 g/cm2, respectively (p > 0.05). This study provides evidence that while the hypertensive resistance arterial segments are not able to produce more tension than normotensive arterial smooth muscle, they are able to narrow faster and narrow more. The latter would result in increased resistance and could result in increased blood pressure.