Vascular Abnormalities in Essential Hypertension

Abstract

Arterial hypertension is a very common disease and an important risk factor for cardiovascular disease. Patients with arterial hypertension are characterized by functional and structural vascular abnormalities. Vascular endothelium plays a fundamental role in modulating vascular tone and structure. The physiological production of the relaxing factors including nitric oxide, prostacyclin and hyperpolarizing relaxing factors protects the vessel wall by antagonizing the first pathogenetic steps of atherosclerosis and thrombosis. Endothelial cells may also produce endothelium-derived contracting factors. The principal component of these contracting factors is endothelin-1, which promotes the growth of the smooth muscle cells and has a vasoconstrictive and blood pressure raising effect. Defective nitric oxide production is already detectable in normotensive offspring of hypertensive patients and young essential hypertensives. A dysfunctional endothelium due to reduced nitric oxide availability associated with an increased production of oxidative stress and vasoconstricting factors is considered as an early indicator of atherothrombotic damage and of cardiovascular events also in patients with arterial hypertension. Moreover, patients with arterial hypertension are also characterized by increased arterial stiffness. This parameter, known as a sign of cardiovascular risk since the 19th century, has been shown to be a predictor of adverse cardiovascular outcome and its measurement in hypertensive patients is suggested by the European guidelines for the diagnosis and treatment of hypertension.

Pathophysiological Contribution of Vascular Function to Baroreflex Regulation in Hypertension

“…30 In contrast, FMD reflects endothelial NO bioavailability, and increased arterial elasticity derived from increased endothelial NO bioavailability may increase BRS. 18 Chapleau et al reported that NO itself directly decreases baroreceptor activity, 31 whereas others reported that NO production in the brain increases BRS. 17 In addition, prostacyclin increases baroreceptor activity and oxygen free radicals decrease baroreceptor activity, 19,20 both being substances related to endothelial function.…”

“…9, 10 In contrast, FMD reflects the endothelial nitric oxide (NO) bio-availability, and NO directly contributes to baroreflex regulation in the brain, besides also contributing indirectly via its effect on arterial elasticity, which is a factor influencing barosensory vessel stretch. 17, 18 Furthermore, endothelial function-related substances such as prostacycline or oxygen free radicals may also directly modulate BRS. 19, 20 The significance of the association of AI/CBP or FMD with BRS, however, has not been fully clarified.…”

“…Immediately after this measurement, the left radial arterial waveform was recorded using an arterial applanation tonometry probe incorporating an array of 40 micropiezoresistive transducers (HEM-9010AI; Omron Healthcare). 17, 18 Then, the first and second peaks of the peripheral systolic pressure (SP1 and SP2) and peripheral diastolic blood pressure (DBP) were automatically detected using the fourth derivatives for each radial arterial waveform, and averaged. rAI was calculated as follows: (SP2−DBP)/(SP1−DBP)×100(%).…”

Intravital Förster resonance energy transfer imaging reveals elevated [Ca2+]i and enhanced sympathetic tone in femoral arteries of angiotensin II‐infused hypertensive biosensor mice

“…Secondly, contractile activation and diameter of FAs were known to be under continuous control of SNA , a characteristic that could help reveal CNS-induced changes in SNA in hypertension. Finally, conduit arteries are of interest because they are importantly involved in the pathophysiology of hypertension, where increased conduit stiffness (possibly due to increased contractile activation) contributes to increased cardiac work (Sparks et al 2011;Sudano et al 2011).…”

“…Thus, [Ca 2+ ] i in FA may reflect some of the systemic factors involved in altering diameter of the true resistance vessels, the small arteries and arterioles. Indeed, in human essential hypertension, conduit arteries such as FA are stiffer than normal, and this contributes to the pathology of hypertension, causing increased arterial pulse wave velocity and increased cardiac work (Sparks et al 2011;Sudano et al 2011).…”