Effect of Hypertension on Arterial Wall Electrolytes During Desoxycorticosterone Administration

Tobian, Louis; Redleaf, Paul D.

doi:10.1152/ajplegacy.1957.189.3.451

Cited by 54 publications

(14 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…35,36 Tobian and Redleaf 37 have proposed that aldosterone affects salt and water balance in vascular cells and thereby influences vessel lumen size. We have reported that vascular 11␤-HSDI and mRNA were decreased in DS rats.…”

Section: Discussionmentioning

confidence: 99%

Renal 11β-Hydroxysteroid Dehydrogenase in Genetically Salt-Sensitive Hypertensive Rats

1998

View full text Add to dashboard Cite

Abstract-Renal 11␤-hydroxysteroid dehydrogenase II (11␤-HSDII) converts glucocorticoids into inactive metabolites and plays an important role in controlling blood pressure and sodium retention. To examine whether this enzyme may be involved in the pathophysiology of salt-sensitive hypertension, we determined 11␤-HSDII activity and mRNA levels in the blood vessel and kidney of Dahl Iwai salt-sensitive (DS) rats and Dahl Iwai salt-resistant (DR) rats. Urinary free corticosterone:free 11-dehydrocorticosterone ratio was measured to estimate renal 11␤-HSD activity. Vascular 11␤-HSDII activity was expressed as percent conversion of [ 3 H]corticosterone to [ 3 H]11-dehydrocorticosterone in homogenized mesenteric arteries. 11␤-HSDII mRNA was estimated with the use of competitive polymerase chain reaction (PCR). Renal 11␤-HSDII activity and mRNA levels were significantly decreased in 8-and 12-week-old high salt DS rats compared with DR, Sprague-Dawley (SD), or low salt DS rats of the same age. Decreased 11␤-HSDII activity and mRNA levels in mesenteric arteries were observed in 8-and 12-week-old high salt DS rats. Urinary excretion of 11␤-HSDII inhibitory factors was measured by inhibition of enzyme activity in microsomes from human kidney. The urinary inhibitors were significantly increased in 8-and 12-week-old high salt DS rats compared with DR, SD, or low salt DS rats of the same age. There were no significant differences in 11␤-HSDII activity and mRNA levels in mesenteric arteries and kidney or in urinary inhibitors between 4-week-old DS, DR, and SD rats. These results indicate that 11␤-HSDII may play a role in salt sensitivity and development of hypertension in the DS rat.

show abstract

Section: Discussionmentioning

confidence: 99%

Renal 11β-Hydroxysteroid Dehydrogenase in Genetically Salt-Sensitive Hypertensive Rats

1998

View full text Add to dashboard Cite

show abstract

“…In previous studies from our laboratory, we combined DOCA injections with a very low sodium diet and found that there was no elevation of blood pressure whatsoever. 22 Moreover, in sheep given DOCA hypertension, the switch to a very low NaCl diet causes a drop of blood pressure to normal levels and also does away with the exaggerated thirst that usually accompanies DOCA-salt hypertension. 23 Moreover, the institution of the low salt diet also diminishes the increased NaCl appetite that the sheep had when they were taking DOCA and NaCl.…”

Section: Evidence That the Central Nervous System Is Involved In Minementioning

confidence: 99%

Aqueduct block markedly reduces mortality and hypertension in post-deoxycorticosterone acetate Dahl salt-resistant rats.

Lee

Tobian

1991

Hypertension

View full text Add to dashboard Cite

When Dahl salt-resistant (DR) rats are given mild post-deoxycorticosterone acetate (DOCA) hypertension, they will have, within 8 weeks, a 53% mortality on a high NaCI diet, without a rise of blood pressure. Forty-two DR rats were given DOCA in silicone (250 mg/kg) and 1% NaCI to drink. After 4 weeks, the DOCA and 1% saline were removed and replaced with a low NaCI diet and tap water. One week later, they were divided into two groups perfectly matched for blood pressure (154 mm Hg). One group had the aqueduct of Sylvius blocked with silicone and epoxy materials; the other group had a sham block. After 4 more recovery weeks on a low NaCI diet, blood pressure averaged 171 mm Hg in sham rats and 147 mm Hg in truly blocked rats (/7<0.0001). Thus, the aqueduct block prevented most of the post-DOCA hypertension and permitted a strong post-DOCA recovery from the acute DOCA hypertension. The rats with the sham block had an actual rise in blood pressure during the post-DOCA recovery period. The vicious cycle leading to permanent post-DOCA NaCI hypertension was broken by the aqueduct block. Then both groups began an 8% high NaCI diet, and after 4 weeks, blood pressure averaged 184 mm Hg in sham and 155 mm Hg in truly blocked rats (/?<0.0001). After 12 weeks on 8% NaCI, all sham rats had died (28 of 28), whereas only one of 14 truly blocked rats had died (93% reduction in mortality,/7< 0.0001). The urinary albumin/creatinine ratio was 36 in sham rats versus only 14 in truly blocked rats (-62%, p<0.0001). The dry heart weights averaged 431 mg in the sham rats versus 310 mg in the truly blocked rats (-28%,p<0.05) even though the body weight of the sham rats averaged 6% less on the high NaCI diet In the post-DOCA NaCI period, it is likely that structural changes linger on in the third brain ventricle region, leading to post-DOCA hypertension and progression of renal lesions. An aqueduct block produces hydrocephalus of the third ventricle and thereby reverses the lingering post-DOCA structural effects, thus greatly reducing blood pressure, mortality rate, cardiac hypertrophy, and urinary albumin. (Hypertension 1991;17:1197-1203) A high NaCI diet is associated with the development of human hypertension, 1 a cause of L. cardiovascular morbidity and mortality in industrialized countries. Although a high NaCI diet is a well-known causal factor in increased blood pressure, understanding the relation between the high dietary NaCI intake and the increased blood pressure is still controversial. The structures surrounding the third brain ventricle are vital for maintenance of normal body fluid homeostasis and cardiovascular responses. Our previous study in Dahl salt-sensitive (DS) rats showed that hydrocephalus produced by blocking the cerebral aqueduct significantly attenuates the rise of blood pressure and the mortality associated with high NaCI diets.2 Other studies have also shown that the anteroventral third ventricle (AV3V) region is a major location for sodium-related receptors and is involved in salt-sensitive hypertension. -10 ...

show abstract

“…In the present study the sodium content was significantly increased but potassium was not. In the previous studies on the rat aorta, the chloride content was either not increased at all or increased only slightly and to a lesser degree than the increase in sodium (2)(3)(4)(5)(6). The present results would agree better with the latter pattern of change.…”

Section: Resultsmentioning

confidence: 85%

“…In previous studies (1)(2)(3)(4)(5)(6) it has been determined that the aortic wall of rats with various forms of experimental hypertension contains an increased amount of sodium, potassium and water per unit of dry weight. The pertinence of these findings to hypertension has always been somewhat in question, since the aorta does not contribute much to the total peripheral resistance.…”

mentioning

confidence: 99%

Sodium and Potassium in the Walls of Arterioles in Experimental Renal Hypertension*

Tobian¹,

Janecek²,

Tomboulian³

et al. 1961

J. Clin. Invest.

Self Cite

View full text Add to dashboard Cite

In previous studies (1-6) it has been determined that the aortic wall of rats with various forms of experimental hypertension contains an increased amount of sodium, potassium and water per unit of dry weight. The pertinence of these findings to hypertension has always been somewhat in question, since the aorta does not contribute much to the total peripheral resistance. In the normal circulation most of the peripheral resistance is provided by the arterioles, and hypertension is accompanied by a narrowing of these arterioles. Hence an analysis of the arterioles themselves would be expected to give more pertinent information concerning the pathogenesis of hypertension. This was attempted in the present experiment.The present study was also designed to offset another possible cause of misinterpretation. When an animal becomes hypertensive, the walls of the arterioles become thicker; some of this thickening is probably related to an increased content of acid mucopolysaccharides, which are known to bind sodium (7). In the present experiment a large number of rats was made hypertensive and thickening of the arterioles occurred in all of them. Half the hypertensive rats were then "cured" of their elevated blood pressure by removing the clip which narrowed their renal artery. We were then able to compare the arterioles of hypertensive and normotensive rats, both of which had comparable degrees of arteriolar thickening.Thus, the present experiment largely overcomes two weaknesses of previous studies. First, electrolytes are estimated in arterioles rather than arteries. Second, there is a similar degree of hypertrophy in both normotensive and hypertensive arterioles.* Supported by a grant from the American Heart Association and by Grant no. H2008, National Heart Institute, United States Public Health Service. METHODSA number of Wistar rats was made hypertensive by narrowing one renal artery with a clip and removing the opposite kidney. Seven months after the original operation, the rats with moderate to severe hypertension were culled out and divided into two groups which were evenly matched for arterial pressure. In one of the two groups, an operation was performed on each rat to remove the clip which narrowed the renal artery. On the rats of the other group, a similar sham operation was done but the clip was left intact. Exactly 7 days after either type of operation, the blood pressure was carefully determined on each rat with the microphonic method (8), and a number of mesenteric arterioles was removed for analysis with the aid of a stereomicroscope. The arterioles of completely normal rats of the same age were also analyzed concomitantly. The arterioles were handled in such a way that the lumen was free of blood before excision of the vessel. As little adventitia as possible was included in the tissue sample. The arterioles in the samples varied in outer diameter from about 25 to 140 A. By measuring serial cross sections of the arterioles, it was possible to compute the fraction of the total arteriolar sample which ...

show abstract

Effect of Hypertension on Arterial Wall Electrolytes During Desoxycorticosterone Administration

Cited by 54 publications

References 0 publications

Renal 11β-Hydroxysteroid Dehydrogenase in Genetically Salt-Sensitive Hypertensive Rats

Renal 11β-Hydroxysteroid Dehydrogenase in Genetically Salt-Sensitive Hypertensive Rats

Aqueduct block markedly reduces mortality and hypertension in post-deoxycorticosterone acetate Dahl salt-resistant rats.

Sodium and Potassium in the Walls of Arterioles in Experimental Renal Hypertension*

Contact Info

Product

Resources

About