Angiotensin vascular other smooth muscle

Peptides are used by most tissues for cell-to-cell communication. As noted in Chapters 6 and 21, they play important roles in the autonomic and central nervous systems. Several peptides exert important direct effects on vascular and other smooth muscles. These peptides include vasoconstrictors (angiotensin II, vasopressin, endothelins, neuropeptide Y, and urotensin) and vasodilators (bradykinin and related kinins, natriuretic peptides, vasoactive intestinal peptide, substance P, neurotensin, calcitonin gene-related peptide, and adrenomedullin). This chapter focuses on the smooth muscle actions of the peptides. 

The heart, as an endocrine organ itself, secretes the atrial natriuretic peptide, which has several important influences on the cardiovascular system. In addition to atrial natriuretic peptide, catecholamines, thyroid hormones, mineralocorticoids, sex steroids, and angiotensin II are other hormones also known to exert their effects on the cardiovascular functions and blood pressure. Hormones regulate the contraction and dilatation of the vascular bed. They may also affect the contraction of other smooth muscles other than the vascular smooth muscle. Oxytocin stimulates contraction of the myoepithelium in the mammary gland that is necessary for milk ejection. 

Vascular endothelium and smooth muscle play important roles in regulating blood vessel tone and BP. These regulating functions are mediated through vasoactive substances that are synthesized by endothelial cells. It has been postulated that a deficiency in the local synthesis of vasodilating substances (e.g., prostacyclin and bradykinin) or excess vasoconstricting substances (e.g., angiotensin II and endothelin I) contribute to essential hypertension, atherosclerosis, and other diseases. 

The endothelin peptides are potent vasoconstrictors that may be involved in heart failure pathophysiology through a number of mechanisms. Endothelin-1 (FT-1), the best characterized of these peptides, is synthesized by endothelial and vascular smooth muscle cells, with the release of ET-1 enhanced by NE, angiotensin II, and inflammatory cytokines. Like other peptides and hormones described earlier, ET-1 plasma concentrations are elevated in heart failure and... 

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