ABSTRACT
More than 100 years have passed since conventional blood pressure measurements became available.1 Soon after the method was reported, the existence of a hypertensive agent, now known as renin, was reported.2 Since then laboratory investigations as well as clinical and epidemiological studies have been carried out in hypertension research and have been advancing in an exponential fashion.3 Since the 1950s, several circulating regulatory peptides, both hypertensive and hypotensive, have been discovered. Blood circulates by the pressure force generated by the cardiac output and peripheral resistance. Each of these primary determinants of the blood pressure is determined by the interaction of an exceedingly complex array of factors including vasoactive peptides. Several peptides directly regulate peripheral resistance such as angiotensin II (Ang II),4
which are vasoconstrictive, and atrial natriuretic peptide,8 calcitonin gene-related peptide (CGRP),9
vasoactive intestinal peptide,10 and adrenomedullin (ADM),11 which are vasodilators. Also, there are volumeregulating peptides such as atrial natriuretic peptide,12
vasopressin,13 and ADM.14 Besides these direct actions, peptides may regulate peripheral resistance and cardiac output indirectly. Peptides may interact with each other as well as regulate humoral factors such as sympathetic nerve activity, nitric oxide (NO), steroid hormones and prostaglandins. It is critical to determine the mosaic of interactions between these agents to determine the physiological role of newly found factors. In this chapter we will focus on NPY, calcitonin, CGRP, and ADM and their mechanism(s) in regulating blood pressure and their effects on end organ damage produced by hypertension.
