Symptoms of renal hypertension

Acute renal parenchymal disease causes high blood pressure is the main mechanism of sodium retention , increased blood volume , blood pressure decreased diuretic often make even normal . The pathogenesis of hypertension, chronic renal disease , but more complicated by a variety of factors .
Factor 1 . Cause sodium retention , increased blood volume
( 1 ) leads to increased blood volume : there are factors that can cause sodium retention : ① GFR (glomerular filtration rate, GFR) decreased sodium and water excretion decreased ; ② renin - angiotensin - aldosterone system activation , aldosterone promote distal tubule and collecting duct sodium reabsorption ; ③ sympathetic nervous system activation , and promote proximal tubular reabsorption of sodium ; ④ NO (nitric oxide, NO) decreased production , tubular natriuresis decrease ; ⑤ renal function insufficiency leading to insulin resistance, increased insulin levels , stimulation of the sodium pump (Na-K-ATP enzyme ) increased proximal tubular reabsorption of sodium . Sodium retention can lead to a significant volume of hypertension ( Figure 1 ) .
( 2 ) result in increased vascular resistance : the following mechanisms may lead to an outer peripheral and renal arteries, vascular resistance increased : ① renin - angiotensin - aldosterone system activation , activation of the sympathetic nervous system and endothelin synthesis, both stimulate vasoconstriction ; ② NO decreased production , antagonize vasoconstrictor factors weakened ; ③ GFR decline resulted in increased secretion of parathyroid hormone , quinoline Pakistan due to the release of endogenous extracellular volume expansion stimulated by parathyroid hormone and quinoline Pakistan can increase the concentration of intracellular Ca2 promote vasoconstriction and increase the muscle wall of the vasoconstrictor factor sensitivity ; ④ insulin resistance, high insulin levels stimulate vascular smooth muscle hypertrophy , vascular response enhancement, wall thickening , luminal narrowing, increased vascular resistance. These factors could lead to resistance to hypertension.
In renal hypertension , the mere volume of hypertension or hypertension pure resistance are rare , most patients department two kinds of risk factors coexist. Compared with essential hypertension, renal hypertension volume factors often more obvious.
Can be learned from the above description , regardless of volume or resistance of hypertension , are associated with many related neurohormonal factors involved , briefly summarized in Table 2 .
2 factors that lead to high blood pressure
( 1 ) the renin - angiotensin - aldosterone system (rennin-angiotensin aldosterone system, RAAS) activation : a lot of information has been confirmed in the occurrence and development of RAAS plays an important role in renal hypertension , renal parenchymal disease missing the blood can lead to RAAS activation. Angiotensin Ⅱ (angiotensin Ⅱ, A Ⅱ) can directly stimulate vasoconstriction , but also by increased central sympathetic activity , and acting on the sympathetic nerve endings to promote the release of catecholamines , further vasoconstriction ; aldosterone increases the distal tubule and collecting duct sodium reabsorption , increased sodium retention . Thus , RAAS activation involved in the resistance of both , but also to participate in the volume of hypertension .
( 2 ) enhanced sympathetic activity : Sympathetic also play an important role in the pathogenesis of renal hypertension . When passing through the renal parenchymal renal diseases sympathetic reflex (afferent renal reflexes) activation , A Ⅱ will also benefit from an increase in the central and peripheral increase its activity. The sympathetic nervous system activation stimulated vasoconstriction, increased vascular resistance ; promote proximal tubular reabsorption of sodium , increased blood volume, and therefore able to participate in both the resistance and the volume of hypertension . Activation of the sympathetic nervous system and renal vasoconstriction can , decreased renal blood flow and stimulate
Renin secretion, further weight gain RAAS activation hypertension .
( 3 ) the release of endogenous digitalis- like substance : with digitalis antibodies cross from the reaction of endogenous digitalis -like substance (endogenous digitalislike substance, EDIS) has the following characteristics : inhibition of Na-K-ATP enzyme , natriuresis . When renal parenchymal disease causes extracellular volume expansion , which can reflect the brain to stimulate the hypothalamus to release EDIS, inhibition of proximal tubular epithelial cell Na-K-ATP enzyme , reducing sodium reabsorption , since natriuresis effect . However , on the other hand the inhibition of vascular smooth muscle EDIS Na-K-ATP enzyme , increased intracellular sodium concentration , reduced sodium transmembrane gradient , and so reduce the voltage-dependent switching Na/Ca2 Ca2 channels depolarization within the cytoplasmic Ca2 therefore increase , which promotes the resistance of hypertension .
( 4 ) ET : ET is the strongest ever found in vivo vasoconstrictor peptide , it is possible through endocrine pathways , as well as autocrine and paracrine pathways play a role. Endothelin stimulates vasoconstriction ; promote RAAS activation ; reduce renal blood flow and GFR, reduce urinary sodium excretion. Therefore , it may be involved in the pathogenesis of renal hypertension from both resistance and volume .
( 5 ) arginine vasopressin : arginine vasopressin to normal body and little effect on blood pressure in patients with essential hypertension , but clinical trials have indicated that chronic renal failure who applied to arginine vasopressin antagonists can effectively decrease blood pressure , suggesting that arginine vasopressin vasoconstrictor effect by those involved in renal hypertension . However, this observation is certainly still need more research and a clear mechanism.

( 6 ) reduced antihypertensive factor : renal factors can produce a variety of blood pressure , such as prostaglandin E2 and I2, bradykinin ( distal renal tubular epithelial cells kallikrein , and then the plasma kininogen into bradykinin ) , atrial natriuretic peptide, brain natriuretic peptide , NO and medulla buck fat and so on. As former Syria , renal parenchymal disease N0 decreased production , antagonize vasoconstriction diminished capacity , but also to reduce NO reduce renal tubular sodium excretion , increased sodium retention , and therefore it from two aspects involved in the resistance and the volume of hypertension . However, they have not been involved in these other antihypertensive factor conclusive evidence of renal parenchymal hypertension .