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Cellular calcium regulation in hypertension.

K Hermsmeyer¹, P Erne

¹Chiles Research Institute, Providence Medical Center, Portland, Oregon 97213.

American Journal of Hypertension

|August 1, 1989

Summary

Vascular muscle cells in spontaneously hypertensive rats (SHR) show an enhanced proportion of sustained (L-type) calcium channels compared to Wistar-Kyoto rats (WKY). This difference in calcium channel activity may contribute to hypertension.

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Area of Science:

Cardiovascular Physiology
Cellular Biology
Hypertension Research

Background:

Vascular muscle cells possess transient (T) and sustained (L) calcium channels, distinguishable by dihydropyridine calcium antagonists.
Spontaneously hypertensive rats (SHR) exhibit hypertension, making their vascular cells a model for studying cardiovascular differences.

Purpose of the Study:

To investigate the ratio of T/L calcium channels in isolated vascular muscle cells from SHR and WKY rats.
To compare intracellular calcium (Ca2+) release and distribution in vascular cells between SHR and WKY strains.

Main Methods:

Quantitation of Ca2+ currents and intracellular Ca2+ release in isolated azygous venous cells.
Utilizing a digital photon-counting camera and Fura-2 fluorescence to analyze subcellular Ca2+ distribution.
Comparing cells from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).

Main Results:

Total transmembranous Ca2+ current did not differ between SHR and WKY rats.
Vascular muscle cells from SHR showed an enhanced proportion of Ca2+ currents carried by L-type channels.
SHR cells exhibited higher intracellular Ca2+ levels upon stimulation, particularly at the cell periphery, with Ca2+ release primarily from the sarcoplasmic reticulum.

Conclusions:

Fundamental differences exist in vascular muscle cells between SHR and WKY rats concerning calcium channel function.
Altered calcium channel activity, modulated Ca2+ release, and Ca2+ uptake are implicated in the hypertension of SHR.
These findings highlight the critical role of calcium handling in the pathophysiology of hypertension.

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