ABSTRACT
Renin is secreted chiefly by the afferent arterioles of the outer cortical nephrons. The activity of the system undergoes a circadian fluctuation with higher levels attained at 4 a.m. Renin release is influenced by many kinds of stimuli. Stretching of the afferent arteriole wall results in an inhibition of renin release. The precise mechanism leading to the macula densa-mediated modulation of renin release has not been as yet clarified. It is possible that macula densa cells act as sensors of sodium, chloride, and other solute presentation rates and/or concentrations within the tubular fluid; the tubular fluid osmolality can also be important. Angiotensin II is the most potent known vasoconstrictor: it is 40 times more effective than an equimolar amount of norepinephrine. Angiotensin III is almost devoid of such a property. The sensitivity of the different vascular beds to angiotensin II is variable.
