[Cardiovascular abnormalities as a cause of hypertension].
This review is an attempt to highlight evidence that may implicate the cardiovascular abnormalities in the pathogenesis of hypertension. Many physiological, pharmacological, and biochemical studies have been conducted in in vitro and in vivo systems. Since blood pressure can rise in response to an increase in cardiac output and/or a rise in peripheral resistance, abnormalities may be present in one or more of the multiple factors that affect these two parameters in hypertension. These multiple factors include various neurohumoral factors. Increased levels of various vasoconstrictor neurohumoral factors have been found in patients with hypertension. Vasoconstrictor neurohumoral factors such as catecholamines, angiotensin II, and endothelin-1 induce vascular smooth muscle cells(VSMCs) proliferation and contraction. On the other hand, vasodilator neurohumoral factors such as natriuretic peptides and adrenomedulin inhibit VSMCs proliferation. Both neurohumoral factors mutually interact and develop hypertension.
Takano
H
H
Department of Medicine III, Chiba University School of Medicine.
Komuro
I
I
D053607:Adrenomedullin; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D002319:Cardiovascular System / Q000503:physiopathology*; D002395:Catecholamines / Q000502:physiology; D002455:Cell Division; D019332:Endothelin-1 / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D007328:Insulin / Q000502:physiology; D016234:Kallikrein-Kinin System / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D045283:Natriuretic Agents / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology; D010455:Peptides / Q000502:physiology; D014661:Vasoconstriction
D002395:Catecholamines; D019332:Endothelin-1; D007328:Insulin; D045283:Natriuretic Agents; D010455:Peptides; D000804:Angiotensin II; D053607:Adrenomedullin; D009569:Nitric Oxide