Kidney juxtaglomerular cells

The kidney contains the major site of renin synthesis, the juxtaglomerular cells in the wall of the afferent arteriole. From these cells, renin is secreted not only into the circulation but also into the renal interstitium. Moreover, the enzyme is produced albeit in low amounts by proximal tubular cells. These cells also synthesize angiotensinogen and ACE. The RAS proteins interact in the renal interstitium and in the proximal tubular lumen to synthesize angiotensin II. In the proximal tubule, angiotensin II activates the sodium/hydrogen exchanger (NHE) that increases sodium reabsorption. Aldosterone elicits the same effect in the distal tubule by activating epithelial sodium channels (ENaC) and the sodium-potassium-ATPase. Thereby, it also induces water reabsotption and potassium secretion. 

Since the discovery of renin over 100 years ago, the RAAS has been extensively studied as a prime target or site of action for many effective antihypertensives.15 Renin is produced and stored in the juxtaglomerular cells of the kidney, and its release is stimulated by impaired renal perfusion, salt depletion, and pr adrenergic stimulation. The release of renin is the rate-limiting... 

Lead may affect renin release from the kidney by affecting calcium ion fluxes in the juxtaglomerular cells, as discussed previously under Cardiovascular Effects. 

The plasma level of angiotensin II is mainly determined by the rate at which renin is released by the kidneys. Renin is synthesized by juxtaglomerular cells, which release it when sodium levels decline or there is a fall in blood pressure. 

Angiotensin II, the primary end product of the renin-angiotensin system, acts on the juxtaglomerular cells to inhibit the release of renin this process is therefore a negative feedback mechanism. The half-life of renin in the circulation is 10 to 30 minutes, with inactivation occurring primarily in the liver. Small amounts of renin are eliminated by the kidneys. Pure human renin... 

Renal blood flow and glomerular filtration are not decreased, although renal resistance is diminished. Like a-methyldopa, it is a useful agent for hypertension complicated by renal disease. Plasma renin activity is reduced by clonidine, presumably as a result of a centrally mediated decrease in sympathetic stimulation of the juxtaglomerular cells of the kidney. 

Angiotensinogen, which is secreted by the liver and circulates in the blood, is converted to the physiologically inactive decapeptide angiotensin I by cleavage of a Leu-Leu peptide bond by the 328-residue renin.d f Its precursor preprorenin is produced in the kidneys by the juxtaglomerular cells as well as in some other tissues and undergoes several... 

Antagonism of ft i-receptors on the juxtaglomerular cells of the kidney that reduce the release of renin. 

Beta-adrenoceptor antagonists are effective antihypertensives and operate partly by blocking /31-receptors on the heart and juxtaglomerular cells of the kidney and partly by central actions which reduce sympathetic activity. 

Increased renin release by juxtaglomerular cells of kidneys... 

Human renin, a 340-amino-acid glycoprotein derived from a larger polypeptide, prorenin, is produced and secreted by the juxtaglomerular cells in the kidney. The presence of only low levels of renin in circulation made human renin difficult to obtain in quantities required for drug screens and structural studies. Therefore, the pepsin family of aspartyl proteases was used for the modeling of human renin in drug... 

Kurtz A, Della BR, Kuhn K. Cyclosporine A enhances renin secretion and production in isolated juxtaglomerular cells. Kidney Int... 

In addition to vasodilatory responses, PGs have a number of other effects in the kidney. For example, PGs stimulate adenylate cyclase in juxtaglomerular cells, resulting in an increase in cAMP production this, in turn, increases renin release. Renin stimulates the release of aldosterone, which increases renal tubular secretion of potassium (Stillman Schlesinger 1990). PGs also enhance tubular excretion of sodium and water (Patrono Dunn 1987). By causing these effects in the kidneys, PGs can alter electrolyte homeostasis. Therefore, other renal side-effects of NSAID therapy can include hyperkalemia, hypernatremia and edema. Often these metabolic changes are not observed in individuals with normal renal function, but in the presence of pre-existing disease they can become clinically significant. 

Tlie p receptors are located mainly in the heart, where they mediate the positive inotropic and chronotropic effects of the catecholamines. They are also found on the juxtaglomerular cells of the kidney, where they are involved in increa.s-ing renin. secretion. The Pz receptors are Irx atcd on smooth muscle throughout the body, where they arc involved in relaxation of the smrxiih muscle, producing such effects as brunchrxlilation and vasodilation. They are also found in the liver, where they promote glycogcnoly.sis. The p, receptor is located on brown adipose tissue and is involved in the stimulation of lipolysis. 

The peptides are normally formed from a precursor molecule - angiotensinogen - an a2-globulin in the blood, by the action of a 340 amino acid glycoprotein called renin, which acts as an aspartyl protease enzyme (see renin inhibitors). Renin, and its precursor protein, are both stored in the juxtaglomerular cells of the kidney, and release is controlled by three different pathways within the kidney sensitive to Na -transport, blood vessel stretch and Pi-adrenoceptor activation, respectively. Overall, activation of the renin-angiotensin systems is hypertensive, but serves to increase renal perfusion. 

Control of renin release from the Icidney is influenced by (1) specialized cells in the distal convoluted tubules called the macula densa function as cliemoreceptors for the concentration of sodium delivered to the distal tubules (2) juxtaglomerular cells functioning as mini pressure transducers sense the renal perfusion pressure in the kidney (3) the sympathetic nervous system that feeds the kidney and catecholamine release and (4) humoral factors such as potassium, atrial natriuretic peptides, and angiotensin II. All of these influences are involved in the normal control of salt and water balance and with diseases of the kidney. Secondary... 

Renin is an enzyme that is stored in the juxtaglomerular cells, which are located in the afferent arterioles of the kidney. The release of renin is modulated by several factors intrarenal factors (e.g., renal perfusion pressure, catecholamines, and angiotensin II) and extrarenal factors (e.g., sodium, chloride, and potassium). 

Juxtaglomerular cells function as a baroreceptor-sensing device. Decreased renal artery pressure and kidney blood flow are sensed by these cells and stimulate secretion of renin. The juxtaglomerular apparatus also includes a group of specialized distal tubule cells... 

Renin A protease that is synthesized by the juxtaglomerular cells of the kidney and secreted into the bloodstream in response to conditions of hypovolemia and hyponatremia. It hydrolyzes circulating angiotensinogen to angiotensin 1. 

The excess production of 11-deoxycorticosterone and corticosterone by infants with an 18-oxidation defect is probably due to an excess production of angiotensin, the stimulant for aldosterone production (M20). Renin, produced by the juxtaglomerular cells in the kidneys, initiates the formation of angiotensin, and a loss of salt causes this substance to be produced in excessive amounts. Evidence for this has been obtained by Ulick et al. (Ul), who found an increased amount of renin in the plasma of their patients during sodium depletion experiments. 

---