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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasodilator responses to acute intra-arterial infusions of K+ are attenuated in dogs with chronic one-kidney perinephritic hypertension in rats with chronic two-kidney Goldblatt hypertension, and in men with essential hypertension. There is evidence that K+ evokes vasodilation by stimulating vascular smooth muscle membrane Na+-K+-activated adenosine triphosphatase, thereby increasing activity of the cellular Na+-K+ electrogenic pump. We therefore proposed that there may be an underlying decrease in the operation of this pump in vascular smooth muscle of hypertensives. The operation of the cellular Na+-K+ pump may be estimated by measurement of rubidium uptake. Thus, so further investigate our hypothesis, we measured 86Rb uptake in small mesenteric arteries and splanchnic veins from 12 dogs with chronic uncomplicated one-kidney perinephritic hypertension and from 12 normotensive control dogs. Vessels were excised under thiamylal anesthesia and incubated in cold medium (plasma or Krebs-Henseleit solution) for sodium loading and then the velocity of 86Rb uptake was estimated in the absence of or in the presence of ouabain, a specific inhibitor of the Na+-K+ pump. In neither arteries nor veins was there evidence for differences between hypertensives and normotensives in the ouabain-insensitive uptake of 86Rb. In contrast, the ouabain-sensitive 86Rb uptake was depressed by 42% in arteries (P less than 0.05) and by 49% in veins (P less than 0.01) from hypertensive dogs, if incubated in the dog's own plasma. These results indicate that the activity of a ouabain-sensitive Na+-K+ pump may be depressed in vascular tissue from dogs with chronic one-kidney perinephritic hypertension. Because the Na+-K+ pump in vascular smooth muscle is probably electrogenic, such an abnormality, by partially depolarizing the muscle cell membrane, would help to account for the elevated vascular resistance found in these dogs.
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PMID:Depressed function of a ouabain-sensitive sodium-potassium pump in blood vessels from renal hypertensive dogs. 13 55

Dr. Skeggs demonstrated the lack of renin dependence in 1-kidney, 1-clip hypertension and elucidated some of the differences between that and Dr. Goldblatt's classic 2-kidney, 1-clip model of hypertension. Studies of these two different types of hypertension have led research in many new directions and helped to reveal the role of the renin-angiotensin system in hypertension and that system's interaction with sodium-induced vasodilation in both animals and humans. More recent research has investigated the processes behind essential hypertension and I present here the proposal that, due to nephron heterogeneity, essential hypertension in humans is parallel in its pathophysiologic processes to Goldblatt hypertension.
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PMID:On the mechanisms and clinical relevance of one-kidney, one-clip hypertension. 174 91

Renal damage is systemic hypertension has traditionally been related to an ischemic glomerular injury secondary to arteriosclerosis and arteriolosclerosis of preglomerular vessels. The use of micropuncture techniques with histopathologic studies have suggested non ischemic mechanisms of renal damage in systemic hypertension. Indeed in experimental models of hypertension which include DOCA-Salt, Goldblatt hypertension or genetic hypertension, the development of glomerular damage is associated with hyperfiltration secondary to increases in flow and pressure to the glomerular capillary. Hyperfiltration as a mechanism of renal damage in human systemic hypertension has not been established. Recent studies from our group have demonstrated lack of renal functional reserve in patients with systemic hypertension, reserve which is reestablished after 3 days of antihypertensive treatment. These data suggest therefore the presence of hyperfiltration as a possible mechanism of renal damage in patients with essential hypertension.
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PMID:[Is the kidney lesion caused by hypertension really ischemic?]. 294 50

In nuclear medicine new trends in the diagnosis of renal function are based on the introduction of new radiopharmaceuticals, improvements in the methodological part of the procedure and precise pharmacological intervention in response to given indications. Tc99m mercaptoacetyltriglycine (Tc99m MAG3) was tested as replacement for I123 orthoiodohippuric acid (I123 oIH) both in the form of a HPLC purified substance and as an impure kit preparation. HPLC purified Tc99m MAG3 clearance determinations in anuric patients showed a low extrarenal excretion amounting to only about 5% of the total clearance in normal patients. Kit preparations yielded about 90% of the labelled product; impurities were pertechnetate, reduced hydrolyzed Tc99m and chemically unidentified labelled products which showed a significantly lower renal, but increased hepatobiliary excretion in comparison with Tc99m MAG3. The renal clearance with kit preparations of Tc99m MAG3 was 55% of the clearance with oIH at a comparable urinary excretion. Significantly higher protein binding and therefore, a decrease in the distribution volume of Tc99m was found in comparison with I123 oIH. No difference was recorded between the two substances with respect to the renogram curves in normal subjects, apart from a modest delay in the elimination of Tc99m MAG3. For clinical purposes kit preparations of Tc99m MAG3 proved equal to I123 oIH. The influence of angiotensin converting enzyme (ACE) inhibitors (captopril) leads to characteristic changes in the renograms of patients with Goldblatt hypertension. Quantitative criteria for the evidence of haemodynamically significant renal artery stenosis were derived from investigations without and with captopril (25 mg) (I123 oIH and Tc99m DTPA) in 21 patients with essential hypertension. The criteria were defined as follows: a delay in peak activity (Tmax) in the I123 oIH captopril renogram exceeding 2 minutes as compared with the baseline value and/or a lower uptake of Tc99m DTPA in comparison with the uptake of I123 oIH (uptake quotient I123 oIH/Tc99m DTPA greater than 1.2). The diagnostic and prognostic potential of the captopril renogram was compared with that of the captopril test by investigating 34 patients with renal artery stenosis (23 uni-, 11 bilateral) (atherosclerosis: 23, fibromuscular hyperplasia: 11). The captopril renogram was positive more often (n = 12) than the captopril test (n = 4) in patients without renal functional impairment of the stenosed kidney. Similar results were obtained with both methods in patients with atrophic kidneys: captopril renography was positive in all cases with a positive captopril test.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[New aspects of nuclear medicine diagnosis of kidney function: improved potential by pharmacologic intervention and quantitative analytic procedures]. 297 26

Increased efferent renal sympathetic nerve activity could facilitate the development of hypertension by shifting the arterial pressure-renal sodium excretion curve to the right. Accordingly, interruption of the renal nerves should prevent the development of hypertension in animal models in which increased sympathetic nervous system activity has been implicated. Renal denervation delays the development of hypertension and results in greater sodium excretion in the Okamoto and New Zealand spontaneously hypertensive rat and in the deoxycorticosterone acetate-salt-treated rat, which suggests that these responses result from, at least in part, loss of efferent renal nerve activity. Similar sympathetically mediated renal vasoconstriction has been implicated in the pathogenesis of early essential hypertension in humans. The efferent renal sympathetic nerves play a diminishing role once hypertension is established in these models. Renal denervation in established one-kidney, one-clip and two-kidney, one-clip Goldblatt hypertension in the rat and chronic coarctation in the dog results in an attenuation of the hypertension. The depressor effect of renal denervation in these models is not caused by changes in renin activity or sodium excretion but is associated with decreased sympathoadrenal activity. These findings suggest that the afferent renal nerves contribute to the pathogenesis of renovascular hypertension by enhancing the activity of the sympathetic nervous system. Interruption of afferent renal fibers also appears to be the mechanism by which renal denervation prevents or reverses the normal increase in arterial pressure seen after aortic baroreceptor deafferentation in the rat.
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PMID:Renal nerves and hypertension: an update. 389 31

Efferent renal innervation is composed of postganglionic sympathetic fibers to the renal arterioles, juxtaglomerular apparatus, and renal tubules. Increased efferent renal sympathetic nerve activity results in increased renal vascular resistance, renin release, and sodium retention. These responses from enhanced renal sympathetic activity contribute to normal cardiovascular homeostasis but could also facilitate the development of hypertension by shifting the arterial pressure-renal sodium excretion curve to the right. Accordingly, interruption of the renal nerves should prevent the development of hypertension in animal models in which increased sympathetic nervous system activity has been implicated. Renal denervation delays the development of hypertension and results in greater sodium excretion in the Okamoto and New Zealand spontaneously hypertensive rat and in the DOCA-salt-treated rat, suggesting that these responses are due, at least in part, to loss of efferent renal nerve activity. Similar sympathetically mediated renal vasoconstriction has been implicated in the pathogenesis of early essential hypertension in man. Recent studies indicate that the kidney is a sensory organ with mechano-receptive and chemoreceptive afferent renal nerves involved in renorenal and cardiovascular regulation. Renal denervation in established one-kidney one-clip and two-kidney one-clip Goldblatt hypertension in the rat and chronic coarctation in the dog results in an attenuation of the hypertension. The depressor effect of renal denervation in these models is not due to change in renin activity or sodium excretion but is associated with decreased activity of the sympathetic nervous system. These findings suggest that the afferent renal nerves contribute to the pathogenesis of renovascular hypertension by enhancing the activity of the sympathetic nervous system. The role of the afferent renal nerves in renovascular hypertension in humans warrants further study.
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PMID:Renal nerves in the pathogenesis of hypertension in experimental animals and humans. 634 99

As the kidneys so importantly contribute to longterm blood pressure control, and decisively to e.g. Goldblatt hypertension, it is often assumed that they are "prime movers" also in most variants of primary hypertension. The "pros and cons" of such a view are briefly discussed, and not least because strategies in therapy and preventive measures in man greatly depend on the nature, and major sites of expression, of the polygenetic predisposition. It is emphasized how the predisposing elements usually seem to exert their main influences via decidedly extra-renal parts of cardiovascular control systems in general, though soon leading to secondary "upward resetting" of the renal barostat function concerning both salt-water excretion and the renal pressure-regulating hormones. In SHR, for example, all proximal systemic resistance vessels, including the renal preglomerular ones, show an intrinsic tendency towards structural upward resetting quite early in life. Further, already early common variants of human primary hypertension, as well as SHR, exhibit an evidently "primary" central hyper-reactivity to psychosocial stimuli. Via neuro-hormonal pressor and growth-promoting effects such in principle extra-renal influences soon induce the same type of cardiovascular and renovascular structural upward resettings. Therefore the transfer of such kidneys to normotensive organisms here induces hypertension because of the prevailing preglomerular resistance increase, which easily gives the impression that these kidneys must have been the cause of hypertension in the donor organism as well.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Kidneys and primary hypertension--initiators, stabilizers or/and victim-aggravators? 799 43