Effects of anti-hypertensive drugs on vessel rarefaction

Abstract

The microcirculation largely determines peripheral vascular resistance and substantially contributes to arterial hypertension. In both human arterial hypertension and animal models of hypertension, genetic, fetal and other mechanisms associated with hypertension can reduce the formation and number of microvessels (i.e. parallel-connected arterioles and capillaries). Impaired formation of microvessels (impaired angiogenesis) and microvascular rarefaction can, on the other hand, contribute to increased peripheral resistance and raise blood pressure. Interestingly, drugs targeting the renin-angiotensin-aldosterone system (i.e. angiotensin-converting enzyme inhibitors and AT(1) receptor blockers) induce angiogenesis in vivo in the majority of animal studies. Furthermore, recent clinical studies demonstrate that long-term antihypertensive treatment increases capillary density in the skin of hypertensive patients without diabetes. These effects of angiotensin-converting enzyme inhibitors and AT(1) receptor blockers can be mediated by activation of bradykinin pathways, resulting in the generation of vascular endothelial growth factor, nitric oxide and, consequently, angiogenesis. In conclusion, specific antihypertensive drugs can induce angiogenesis and reduce or even reverse microvascular rarefaction. This might improve target organ damage in, and slow the development of, hypertension.