Renal vascularization

Cyclosporine and tacrolimus are calcineurin inhibitors that are administered as part of immunosuppressive regimens in kidney, liver, heart, lung, and bone marrow transplant recipients. In addition, they are used in autoimmune disorders such as psoriasis and multiple sclerosis. The pathophysiologic mechanism for ARF is renal vascular vasoconstriction.41 It often occurs within the first 6 to 12 months of treatment, and can be reversible with dose reduction or drug discontinuation. Risk factors include high dose, elevated trough blood concentrations, increased age, and concomitant therapy with other nephrotoxic drugs.41 Cyclosporine and tacrolimus are extensively metabolized by... 

Hopkins PN, Lifton RP, Hollenberg NK, Jeunematre X, Hallouin MC, Skuppin J, Williams CS, Dluhy RG, La-louel JM, Williams RR, Williams GH. Blunted renal vascular response to angiotensin II is associated with a common variant of the angiotensinogen gene and obesity. J Hypertens 1996 14 199-207. 

NK. Blunted renal vascular response to angiotensin II is associated with a common variant of the angiotensinogen gene and obesity. J Hypertens 1996 14 199-207. 

Vasopressin causes vasoconstrictive effects that, unlike adrenergic receptor agonists, are preserved during hypoxia and severe acidosis. It also causes vasodilation in the pulmonary, coronary, and selected renal vascular beds that may reduce pulmonary artery pressure and preserve cardiac and renal function. However, based on available evidence, vasopressin is not recommended as a replacement for norepinephrine or dopamine in patients with septic shock but may be considered in patients who are refractory to catecholamine vasopressors despite adequate fluid resuscitation. If used, the dose should not exceed 0.01 to 0.04 units/min. 

Together with the increase in cardiac output, renal blood flow is also increased with a significant decrease in renal vascular resistance(10). 

In the same study, neither the renal blood flow nor the renal vascular resistances were found to be affected by P840 (data not shown). 

Pharmacology Initially, clonidine stimulates peripheral -adrenergic receptors producing transient vasoconstriction. Stimulation of alpha-adrenergic in the brain stem results in reduced sympathetic outflow from the CNS and a decrease in peripheral resistance, renal vascular resistance, heart rate, and blood pressure. Pharmacokinetics Blood pressure declines within 30 to 60 minutes after an oral... 

For a few compounds claims have been made that they may even be selective for a particular vascular bed. Examples are nimodipine (cerebral vessels), nisoldipine (coronary arteries), and manidipine (renal vascular bed). Although potentially attractive, the clinical evidence for such a selectivity is so far not convincing. 

D3 (DAi), D5 Brain effector tissues, especially smooth muscle of the renal vascular bed Stimulation of adenylyl cyclase and increased cAMP... 

Intravenous administration of dopamine promotes vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels, via activation of Di receptors. Activation of the Di receptors in the renal vasculature may also induce natriuresis. The renal effects of dopamine have been used clinically to improve perfusion to the kidney in situations of oliguria (abnormally low urinary output). The activation of presynaptic D2 receptors suppresses norepinephrine release, but it is unclear if this contributes to cardiovascular effects of dopamine. In addition, dopamine activates Bj receptors in the heart. At low doses, peripheral resistance may decrease. At higher rates of infusion, dopamine activates vascular a. receptors, leading to vasoconstriction, including in the renal vascular bed. Consequently, high rates of infusion of dopamine may mimic the actions of epinephrine. 

Reduction in arterial blood pressure by clonidine is accompanied by decreased renal vascular resistance and maintenance of renal blood flow. As with methyldopa, clonidine reduces blood pressure in the supine position and only rarely causes postural hypotension. Pressor effects of clonidine are not observed after ingestion of therapeutic doses of clonidine, but severe hypertension can complicate a massive overdose. 

The renal vascular receptor functions as a stretch receptor, with decreased stretch leading to increased renin release and vice versa. The receptor is apparently located in the afferent arteriole, possibly in the juxtaglomerular cells. Stretch-induced changes in renin release are mediated by changes in Ca2+ concentration in the juxtaglomerular cells. 

Depending on the concentration, volatile anesthetics decrease the glomerular filtration rate and renal blood flow, and increase the filtration fraction. Since renal blood flow decreases during general anesthesia in spite of well-maintained or even increased perfusion pressures (due to increased renal vascular resistance), autoregulation of renal flow may be impaired by these drugs. 

Monster TB, Janssen WM, de Jong PE, de Jong-van den Berg LTPrevention of Renal Vascular End Stage Disease Study Group. Oral contraceptive use and hormone replacement therapy are associated with microalbuminuria. Arch Intern Med 2001 161(16) 2000-5. 

Column C represents a case in which sympathetically mediated renal vascular tone is assumed to be a significant factor in maintaining the elevated pressure, and column D depicts possible changes in the few cases of human essential hypertension in which a continued fall in pressure is noted for some time after sympathectomy, perhaps also on the basis of altered renal blood flow. Column E represents a common result of sympathectomy or adrenergic blockade in renal and essential hypertension this result may or may not be preceded by some early fall in pressure such as illustrated in column C. 

Most cardiovascular reflexes remain intact after administration of methyldopa, and blood pressure reduction is not markedly dependent on maintenance of upright posture. Postural (orthostatic) hypotension sometimes occurs, particularly in volume-depleted patients. One potential advantage of methyldopa is that it causes reduction in renal vascular resistance. 

The rate at which renin is secreted by the kidney is the primary determinant of activity of the renin-angiotensin system. Renin secretion is controlled by a variety of factors, including a renal vascular receptor, the macula densa, the sympathetic nervous system, and angiotensin II. 

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