Humoral trophic influence on cardiovascular structural changes in hypertension.

Yamori, Yukio; Igawa, Takehiro; Tagami, Motoki; Kanbe, Toshimi; Nara, Yasuo; Kihara, Masahiro; Horie, Rie

doi:10.1161/01.hyp.6.6_pt_2.iii27

Cited by 39 publications

(22 citation statements)

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“…The K., however, was similar to that of cells from the WKY rat. There is abundant evidence for accelerated growth in culture of VSMC from the SHR (9,35,36), and several studies have shown participation of the Na+/H' antiporter in the initiation of cell growth (3,4,37). It is conceivable that increased growth rate in SHR cells may require recruitment of a greater number of antiporters in the plasma membrane or enhancement oftheir activity.…”

Section: Discussionmentioning

confidence: 99%

Kinetic properties of the Na+/H+ antiporter of lymphocytes from the spontaneously hypertensive rat: role of intracellular pH.

Saleh

Batlle

1990

J. Clin. Invest.

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Enhanced activity of the Na+/H' antiporter is increasingly reported as a feature of cells from hypertensive subjects but the intracellular pH (ipH) dependency of its activity has not been examined. This study was designed to characterize the kinetic properties of the Na+/H' antiporter in lymphocytes from adult spontaneously hypertensive rats (SHR) and in those from age-matched normotensive Wistar-Kyoto (WKY) controls. Steady-state ipH, estimated from the measurement of BCECF fluorescence, was significantly lower in lymphocytes from the SHR than in those from WKY rats (7.09±0.02, n = 17 and 7.17±0.03, n = 19, respectively, P < 0.025). The velocity of the antiporter determined from the product of the We conclude that while the ipH of SHR lymphocytes is reduced, the kinetic properties of the Na+/H' antiporter are virtually identical in SHR and WKY lymphocytes. Consequently, a primary abnormality in the activity of this antiporter is not an inherent feature of lymphocytes from the SHR model of genetic hypertension. We propose that the activity of the

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Section: Discussionmentioning

confidence: 99%

Kinetic properties of the Na+/H+ antiporter of lymphocytes from the spontaneously hypertensive rat: role of intracellular pH.

Saleh

Batlle

1990

J. Clin. Invest.

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“…Yamori and colleagues (15,16) demonstrated that VSMC cultured from aortae of 12-and 24-wk SHR and SHR stroke-prone rats proliferated significantly more rapidly than those from agematched Wistar Kyoto (WKY) rats. These investigators also observed that SHR VSMC maintained increased DNA synthesis at any concentration of extracellular Na' ( 15). There have been few other studies that relate abnormalities of VSMC membrane cation transport to altered cell growth.…”

Section: Introductionmentioning

confidence: 99%

Spontaneously hypertensive rat vascular smooth muscle cells in culture exhibit increased growth and Na+/H+ exchange.

Berk¹,

Vallega²,

Muslin³

et al. 1989

J. Clin. Invest.

188

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The cellular mechanisms responsible for abnormalities in spontaneously hypertensive rat (SHR) vascular smooth muscle cell (VSMC) growth and vasoreactivity are not defined. Because Na+/H' exchange, which we have previously demonstrated in cultured VSMC, plays an essential role in mediating growth factor responses, we hypothesized that abnormalities in SHR growth regulation might be reflected in the activity of this transporter. To test this hypothesis, we studied DNA synthesis and Na+/H' exchange (measured as the rate of amiloride-sensitive intracellular alkalinization or Na' influx) in early subcultures (< 6) of aortic VSMC from 12-wk-old SHR and Wistar Kyoto (WKY) animals. Serum-deprived SHR VSMC grew more rapidly in response to 10% serum with an increase in [3Hjthymidine incorporation of 439% compared with 191% in WKY controls. Basal intracellular pH (pHj) values determined by fluorescent pH measurements were 7.37±0.04 and 7.27±0.03 (P < 0.05) in early passage SHR and WKY, respectively. Acid recovery (initial pH1 = 6.8) by SHR VSMC was faster than by WKY VSMC as measured by alkalinization (1.8±0.6 vs. 0.8±0.2 mmol Hf/liter * min, P < 0.05) or by amiloride-sensitive 22Na' influx (14.5±1.2 vs. 4.0±0.5 nmol Na+/mg protein * min, P < 0.05). In comparison to WKY cells early passage SHR VSMC exhibited 2.5-fold greater alkalinization and amiloride-sensitive 22Na' influx in response to 100 nM angiotensin II. During serial passage, WKY cells acquired enhanced Na+/H' exchange and growth rates so that by passage 6, these differences were no longer present. These findings in early cultures of SHR VSMC, removed from the in vivo neurohumoral milieu, suggest that increased Na+/H' exchange in SHR may reflect alterations in Na' homeostasis that might contribute to altered SHR VSMC function such as enhanced growth and vasoreactivity.

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“…50 Also , the factors that regulate fibroblast growth and collagen production may be under separate neurohumoral control from tho e responsible for myocyte hypertrophy. 51 In one clinical study, patients treated with enalapril (n = 7) or nifedipine (n = II) for 6 month had a reduction in left ventricular ma s of 20 %; the regresion in left ventricular hypertrophy was not as ociated with a reduction in left ventricular function. 52 When antihypertensive treatment was withdrawn for 3 weeks , blood pressure returned to hypertensive level .…”

Section: Angiotensin-converting Enzyme Inhibitors and Left Ventriculamentioning

confidence: 99%

Angiotensin‐converting enzyme inhibition, cell growth, and left ventricular hypertrophy in hypertension

Giles

1991

Clinical Cardiology

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Summary: Left ventricular hypertrophy is now recognized as an important risk marker in cardiovascular morbidity and mortal ity. Left ventricular hypertrophy is an integral component of the complex pathophysiology of primary hypertension and results from mechanical, neurohumoral, and genetic factors . The renin-angiotensin system is involved with the production of left ventricular hypertrophy, not only through the effects on systemic arterial blood pressure but also by both direct and indirect effects on myocardial cell growth. The angiotensin-converting enzyme (ACE) inhibitors are effective drugs for reducing blood pressure in primary hypertension . ACE inhibitor therapy is also associated with regression of left ventricular hypertrophy and restoration of normal diastolic and systolic left ventricular function. Regression of left ventricular hypertrophy is associated with improved prognosis . Thus, when left ventricular hypertrophy regression is a goal of antihypertensive treatment, the ACE inhibitors are effective drugs .

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Humoral trophic influence on cardiovascular structural changes in hypertension.

Cited by 39 publications

References 0 publications

Kinetic properties of the Na+/H+ antiporter of lymphocytes from the spontaneously hypertensive rat: role of intracellular pH.

Kinetic properties of the Na+/H+ antiporter of lymphocytes from the spontaneously hypertensive rat: role of intracellular pH.

Spontaneously hypertensive rat vascular smooth muscle cells in culture exhibit increased growth and Na+/H+ exchange.

Angiotensin‐converting enzyme inhibition, cell growth, and left ventricular hypertrophy in hypertension

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