[Cellular calcium, vasoconstriction, hypertension].
The control of vasomotion is a central issue in blood pressure regulation and is a primary goal of antihypertensive therapy. Calcium is the final messenger in the contractile mechanism of vascular smooth and cardiac muscle. Vasoconstrictor agents enhance the entry of Ca++ into vascular myocytes; vasodilators usually depress it. The most recent findings, based on direct measures of intracellular Ca++, have also highlighted the importance of calcium-sensitization mechanisms: vasoconstrictors sensitize the contractile apparatus to Ca++; vasodilators have an opposite effect. Cell calcium control alterations have been reported in different forms of hypertension. An increase in vascular myoplasmic Ca++ and a higher rate of calcium influx through specific, dihydropiridine-sensitive calcium channels have been found in genetic or secondary animal models. In hypertensive patients, an elevation of cytoplasmic Ca++ was noted in the platelets. Since Ca++ is a ubiquitous intracellular messenger, these changes may have profound implications for the pathophysiology of hypertension.
Bruschi
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G
Istituto di Clinica Medica e Nefrologia, Università degli Studi di Parma.
Regolisti
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G
Borghetti
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A
D000818:Animals; D002118:Calcium / Q000502:physiology*; D015220:Calcium Channels / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D015290:Second Messenger Systems / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology*
D015220:Calcium Channels; D002118:Calcium
Calcio cellulare, vasocostrizione, ipertensione.