Presentation on theme: "The Physiology of the Afferent and Efferent Arterioles."— Presentation transcript:
The Physiology of the Afferent and Efferent Arterioles
Role of the Afferent and Efferent Arterioles The kidneys have an autoregulatory system to keep their blood flow and perfusion constant over a wide range of blood pressures. Unlike perfusion of all other organs, perfusion of the kidney is not regulated to maintain organ nutrition but to retain its filtration functions. The glomerular hydrostatic pressure is regulated mainly by the balance of vascular tone in the afferent and efferent arterioles. Owing to this exceptional arrangement of resistance vessels in series, before and after the glomerulus, renal blood flow (RBF) and glomerular filtration rate (GFR) can be regulated independently.
A selective increase in afferent resistance decreases RBF, the blood flow into the glomerulus, and the glomerular filtration pressure, a primary force for plasma ultrafiltration. On the other hand, constriction of the efferent arteriole raises glomerular filtration pressure, thereby maintaining or even increasing GFR despite a drop in RBF and thus causing an increase in filtration fraction (GFR/RBF). The vascular tone of these preglomerular and postglomerular vessels is regulated by several systems, including circulating hormones, paracrine factors, and the renal sympathetic nerves.
Humoral Mechanisms Controlling Afferent and Efferent Arteriolar Resistance Angiotensin II – A potent vasoconstrictor – Causes a rise in filtration fraction – Predominant action on the efferent arteriole Endothelin – The endothelins are vasoconstrictor peptides mediated usually through ET B receptors. – Endothelin-1 (ET-1) causes renal vasoconstriction and a decrease in RBF. – The afferent arteriole is more sensitive to the vasoconstrictor action of ET-1 than the efferent arteriole.
Atrial Natriuretic Peptide – Causes afferent arteriolar vasodilation and efferent arteriolar vasoconstriction. – The greater GFR resulted from a rise in glomerular pressure – ANP has also been shown to reverse noradrenaline-induced afferent vasoconstriction and to potentiate its efferent arteriolar vasoconstriction. – This action of ANP has been suggested to help maintain GFR in heart failure,  in which ANP values are elevated and renal perfusion pressure is reduced. Arginine Vasopressin – Arginine vasopressin (AVP) is a potent vasoconstrictor, particularly in the mesenteric circulation, with less effect on the kidney. – AVP caused a reduction in the lumen diameter of efferent arterioles, an effect blocked by a specific V 1 receptor antagonist, but AVP had no effect on afferent arterioles.
Paracrine Agents Nitric Oxide – NO is a potent vasodilator. – The afferent arteriole is more sensitive than the efferent arteriole to the vasodilator effects of NO. – The main action of NO is to modulate the action of angiotensin. – L-NAME significantly augmented the vasoconstrictor action of angiotensin II in afferent arterioles. Prostaglandins – The major action of prostaglandins is to modulate the actions of vasoconstrictors. – The juxtamedullary afferent arteriolar response to angiotensin II is enhanced by cyclooxygenase inhibition. Adenosine and ATP – Adenosine evokes vasoconstriction. – The vasoconstriction of afferent and efferent arterioles results from activation of A 1 receptors.
Control by the Sympathetic Nervous System The kidney receives sympathetic innervation that extends to the vascular smooth muscle cells, juxtaglomerular renin-secreting cells, and mesangium as well as the proximal and distal tubules and the loop of Henle. The afferent arterioles are threefold more densely innervated than the efferent arterioles. Differential innervation of the afferent and efferent arterioles indicates that the sympathetic nervous system evokes selective changes in preglomerular and postglomerular resistance to regulate GFR and renal function.
Effects of Drugs Calcium Antagonists – Calcium antagonists cause preferential vasodilation of the afferent arteriole. – Action of a calcium antagonist may cause glomerular hypertension that could lead to the progression of renal diseases. ACEI and AT-1 Antagonists – Losartan and captopril increase RBF and GFR and decrease filtration fraction through a reduction in total renal resistance due to a decrease in efferent resistance. Dopamine – Low-dose dopamine causes renal vasodilation. – Dopamine produced dilation of the afferent arterioles and a smaller degree of dilation of the efferent arterioles near the glomeruli.