Question

After returning to the recovery room the valve starts to leak and the blood pressure starts to fall, a patient who was sent open-heart surgery for a replacement of an aortic valve. After the personal starts to infuse norepinephrine to increase the blood pressure, the renal function of the patient starts to decline.

1. What are the mechanisms by which norepinephrine might lower the glomerular filtration rate? Be sure to focus on renal plasma flow and Glomerular Capillary Hydrostatic Pressure.

2. The personal is concerned by his lowered glomerular filtration rate. The elect to try a new treatment, the infusion of atrial natriuretic peptide (ANP). What might be the mechanism by which this would increase GFR?

Answer 1

1 Norepinephrine is very effective in raising arterial blood pressure and, under almost all circumstances, can be titrated to achieve the desired MAP in a given patient. However, since noradrenaline induces vasoconstriction via α-adrenergic stimulation, it may also decrease organ blood flow, if regional vascular beds constrict in excess. In such a scenario, intra-organ vascular resistance would increase proportionately more than perfusion pressure and overall blood flow would decrease, particularly for the kidney

The kidneys are innervated by the sympathetic neurons of the autonomic nervous system via the celiac plexus and splanchnic nerves. Reduction of sympathetic stimulation results in vasodilation and increased blood flow through the kidneys during resting conditions. When the frequency of action potentials increases, the arteriolar smooth muscle constricts (vasoconstriction), resulting in diminished glomerular flow, so less filtration occurs. Under conditions of stress, sympathetic nervous activity increases, resulting in the direct vasoconstriction of afferent arterioles (norepinephrine effect) as well as stimulation of the adrenal medulla. The adrenal medulla, in turn, produces a generalized vasoconstriction through the release of epinephrine. This includes vasoconstriction of the afferent arterioles, further reducing the volume of blood flowing through the kidneys. This process redirects blood to other organs with more immediate needs.
Norepinephrine reduce GFR.

2
ANF acts on the kidney to increase sodium excretion and GFR, to antagonize renal vasoconstriction, and to inhibit renin secretion. In the cardiovascular system, ANF antagonizes vasoconstriction, and shifts fluid from the intravascular to the interstitial compartment. In the adrenal gland, ANF is a powerful inhibitor of aldosterone synthesis. ANF participates importantly in the natriuretic response to acute and chronic volume overload. ANF's property of shifting fluid from the vascular to the interstitial compartment acts as a buffering device, guarding against excessive plasma volume expansion in face of an increased total extracellular fluid volume.ANF exerts a smooth muscle relaxant effect on isolated vessels constricted with various hormonal agonists .ANF also inhibits steroidogenesis, most prominently affecting agonist-induced aldosterone biosynthesis by the adrenal cortex
Guanylyl cyclase (GCA) receptors mediate the effects of ANF by generating cGMP. Clearance receptors remove ANF from the circulation by receptor-mediated endocytosis, and serve as a hormone buffer system to impede large inappropriate fluctuations in plasma levels of ANF. The specific structure-function-dynamics relationships of these receptors serve to modulate the role of ANF in pressure-volume homeostasis.
* ANP increases glomerular filtration rate and glomerular permeability. ANP directly dilates the afferent arteriole and counteracts the norepinephrine induced vasoconstriction of the afferent arteriole