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It has been reported that the increased function of the voltage-dependent calcium channels (VDCC) in the artery is involved in the increase of peripheral resistance in hypertension, and that the sarcoplasmic reticulum (SR) in the artery plays an important role in preventing the development of hypertension via a buffering effect. However, no reports have described the role of VDCC and SR in resistance arterioles in the development or maintenance of hypertension. We investigated the function of VDCC and of SR in the cremaster arterioles of spontaneous hypertensive rats (SHR) and age-matched Wistar Kyoto rats (WKY). The changes in diameter and the intracellular calcium ion concentration ([Ca2+]i) in the microdissected arterioles, using fluorescent dyes, were measured with videomicroscopy. The KCl concentration-response curves were analyzed in 4- to 5- and 7- to 8-week-old SHR and WKY. The changes in the vascular diameter and [Ca2+]i in response to ryanodine, an alpha-1 adrenoceptor, and angiotensin-II stimulation were compared between the 7- to 8-week-old SHR and WKY. We found an increase in the Ca2+ influx by VDCC in the early hypertensive stage, but not in prehypertensive SHR. However, after the onset of hypertension, there were no significant differences from WKY in the SR function mediated by Ca2+-induced Ca2+ release or inositol 1,4,5-trisphosphate-induced Ca2+ release. In conclusion, an increased influx of Ca2+ in the cell membrane, without a buffering effect of SR, was associated with progression of hypertension in the cremaster arterioles of SHR.

In this study, we evaluated the relationship between the endothelium-dependent vasodilation and salt sensitivity in patients with essential hypertension. Fifteen untreated hypertensive male patients (age, 29 to 54 years) were sodium restricted (5 g/day) for 1 week, and placed on a high salt diet (20 g/day) the second week. At the end of each period, measurements of forearm vascular responses to drugs (acetylcholine, 3 to 24 microg/min; sodium nitroprusside, 0.15 to 1.2 microg/min; norepinephrine, 0.15 to 1.2 microg/min; and N(G)-monomethyl-L-arginine [L-NMMA], 1 to 8 micromol/min) were obtained by using strain-gauge venous plethysmography. Subjects were divided into two groups according to the blood pressure response to sodium loading: salt-sensitive hypertensive group (24-h mean increase of arterial pressure > or = 10%; n = 6) and salt-resistant group (< 10%; n = 9). The two groups showed no significant difference in clinical data or mean arterial pressure during low salt intake. The dose-dependent vasodilation induced by acetylcholine was significantly reduced (P < .05) in the salt-sensitive hypertensive patients v the salt-resistant patients regardless of sodium loading. There were no differences between the two groups in response to sodium nitroprusside, norepinephrine, or L-NMMA. These results indicate that vasodilation to acetylcholine is reduced in salt-sensitive hypertensive patients even on restricted sodium diets. This may contribute to blood pressure elevation when sodium intake is increased.

Left ventricular hypertrophy is an adaptive response to long standing hypertension. However, the influence of left ventricular hypertrophy with hypertension on extent of infarct expansion has not been studied. We compared the effects of left ventricular hypertrophy with hypertension on infarct expansion in spontaneously hypertensive rats (SHR, n = 76), Wistar-Kyoto rats (WKY ; n = 46) and spontaneously hypertensive rats treated with delapril, an angiotensin converting enzyme (ACE) inhibitor (SHRD ; n = 39). The survival rates at 7 days after myocardial infarction were 41%, 24%, and 46% for WKY, SHR, and SHRD. The survival rate of SHR was significantly lower than those of both SHRD and WKY (P

To characterize the myogenic response during the development of hypertension, we evaluated the myogenic response of small arteries isolated from the cremaster muscle of spontaneously hypertensive rats (SHR) aged 4-5 and 7-8 weeks, as compared with age-matched Wistar-Kyoto rats (WKY), using an in vitro system. The myogenic response of SHR aged 7-8 weeks (but not those aged 4-5 weeks) significantly exceeded that of WKY. Measurement of intracellular levels of free calcium ([Ca 2+ ] i ) in small arteries of the 7-8-week-old SHR and WKY loaded with a calcium-sensitive dye showed that the increase in [Ca 2+ ] i in SHR was significantly greater than that in WKY during the myogenic response. The inhibitory effects of nitrendipine on the increased myogenic response and [Ca 2+ ] i were greater in SHR. Thus, the myogenic response was enhanced in SHR and may be explained in part by an increase in Ca 2+ entry through the voltage-dependent calcium channel (VDCC). The myogenic response and Ca 2+ entry through the VDCC may be increased in association with the elevation of blood pressure. Am J Hypertens 1998;11:767-773 © 1998 American Journal of Hypertension, Ltd.