Renal–adrenal interrelationships in experimental hypertension

1968 ◽  
Vol 46 (2) ◽  
pp. 179-188 ◽  
Author(s):  
D. Ostrovsky ◽  
F. R. Papsin ◽  
A. G. Gornall
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Renal Artery ◽  
High Blood Pressure ◽  
Salt Intake ◽  
Renal Tissue ◽  
Experimental Hypertension ◽  
Normal Blood Pressure ◽  
Renal Hypertrophy ◽  
High Salt Intake

For several weeks after partial constriction of one renal artery, the fate of this "clipped" kidney seems to exert a determining influence on blood pressure. Rats that remained hypertensive throughout the experiment almost invariably had clipped kidneys averaging 0.16 to 0.22% of body weight. Below 0.1%, this kidney was usually quite atrophic, and its presence was consistent with falling or normal blood pressure. The untouched kidney in such rats was, on the average, heavier in the hypertensive than in the normotensive animals. Since the latter also had less renal tissue on the clipped side, it appears that factors leading to high blood pressure stimulated hypertrophy beyond the level provoked by renoprival factors. In rats on a high salt intake, 5 μg/day of D-aldosterone for 3 months stimulated significant true renal hypertrophy in the absence of a rise in blood pressure. Such hypertrophy was more pronounced in similar rats that had been getting 250 μg DOCA/day for 3 months but were also normotensive. Rats that developed hypertension on this latter regimen had still heavier kidneys. Renal hypertrophy appears to be a prehypertensive phenomenon which persists and can become even more pronounced in hypertension. The highest levels of renal hypertrophy were usually associated with significant adrenal hypertrophy. Endocrine functions may be involved in renal hypertrophy. This concept is discussed in relation to a phospholipid "renin inhibitor" recently isolated from dog and hog kidneys.

High dietary salt intake increases carotid blood pressure and wave reflection in normotensive healthy young men

2011 ◽  
Vol 110 (2) ◽  
pp. 468-471 ◽  
Author(s):  
Mirian J. Starmans-Kool ◽  
Alice V. Stanton ◽  
Yun Y. Xu ◽  
Simon A. McG Thom ◽  
Kim H. Parker ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Body Weight ◽  
Wave Reflection ◽  
Salt Intake ◽  
High Salt ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Salt Intake ◽  
Increased Risk

Dietary salt intake is associated with high brachial blood pressure (BP) and increased risk of cardiovascular disease. We investigated whether changes in dietary salt intake are associated with changes in central BP and wave reflection in healthy volunteers. Ten healthy normotensive male volunteers (22–40 yr) participated in a 6-wk double-blind randomized crossover study to compare a low-dietary salt intake (60–80 mmol sodium/day) with a high-salt intake (low salt intake supplemented with 128 mmol sodium/day) on central BP and wave reflection. Brachial and carotid BP, carotid blood flow velocity, forward (Pf) and backward (Pb) pressure, wave intensity, body weight, and urinary electrolyte excretion were measured at the end of each crossover period. High salt intake significantly increased carotid systolic BP [98 (SD 11) vs. 91 mmHg (SD 13), P < 0.01] and increased wave reflection [ratio of backward to forward pressure (Pb/Pf) 0.13 (SD 0.02) vs. 0.11 (SD 0.03), P = 0.04] despite only small effects on brachial BP [114 (SD 9) vs. 112 mmHg (SD 6), P = 0.1]. Urinary sodium excretion and body weight were also increased following high salt intake. High salt intake disproportionately increases central BP compared with brachial BP as a result of enhanced wave reflection. These effects may contribute to the adverse effect of high dietary salt intake on the risk of cardiovascular disease.

scholarly journals GENETIC INFLUENCE ON THE DEVELOPMENT OF RENOPRIVAL HYPERTENSION IN PARABIOTIC RATS

1969 ◽  
Vol 130 (6) ◽  
pp. 1353-1365 ◽  
Author(s):  
K. D. Knudsen ◽  
J. Iwai ◽  
M. Heine ◽  
G. Leitl ◽  
L. K. Dahl
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Genetic Factors ◽  
Salt Intake ◽  
Renal Hypertension ◽  
Genetic Influence ◽  
High Salt ◽  
Equal Frequency ◽  
High Salt Intake ◽  
Blood Pressures

Rats from two strains with opposite constitutional predisposition to hypertension were joined in parabiosis and one partner was nephrectomized. The influence of genetic factors and of diet on the blood pressures of the two classes of parabionts, operated and intact, indicated that renoprival hypertension occurred with equal frequency in rats from both strains; that the development of renoprival hypertension depended on the influence from an intact S partner, or on a high salt intake, or on both. A nephrectomized S rat developing renoprival hypertension did not induce high blood pressure in its intact R partner. In this respect renoprival hypertension differs from salt and renal hypertension. The findings are interpreted to mean that the hypertensinogenic agent specific for S rats is produced by S kidneys.

Statins reverse renal inflammation and endothelial dysfunction induced by chronic high salt intake

2011 ◽  
Vol 301 (2) ◽  
pp. F263-F270 ◽  
Author(s):  
M. C. Fiore ◽  
P. M. Jimenez ◽  
D. Cremonezzi ◽  
L. I. Juncos ◽  
N. H. García
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Body Weight ◽  
Salt Intake ◽  
High Salt ◽  
Lipid Lowering ◽  
Inflammatory Factors ◽  
Glomerular Volume ◽  
High Salt Intake ◽  
Tgf Β1

High salt intake (HS) is a risk factor for cardiovascular and kidney disease. Indeed, HS may promote blood-pressure-independent tissue injury via inflammatory factors. The lipid-lowering 3-hydroxy 3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors exert beneficial lipid-independent effects, reducing the expression and synthesis of inflammatory factors. We hypothesized that HS impairs kidney structure and function in the absence of hypertension, and these changes are reversed by atorvastatin. Four groups of rats were treated for 6 wk in metabolic cages with their diets: normal salt (NS); HS, NS plus atorvastatin and HS plus atorvastatin. We measured basal and final body weight, urinary sodium and protein excretion (UProtV), and systolic blood pressure (SBP). At the end of the experimental period, cholesterolemia, creatinine clearance, renal vascular reactivity, glomerular volume, cortical and glomerular endothelial nitric oxide synthase (eNOS), and transforming growth factor (TGF)-β1 expression were measured. We found no differences in SBP, body weight, and cholesterolemia. HS rats had increased creatinine clearence, UProtV, and glomerular volume at the end of the study. Acetylcholine-induced vasodilatation decreased by 40.4% in HS rats ( P < 0.05). HS decreased cortical and glomerular eNOS and caused mild glomerular sclerosis, interstitial mononuclear cell infiltration, and increased cortical expression of TGF-β1. All of these salt-induced changes were reversed by atorvastatin. We conclude that long-term HS induces inflammatory and hemodynamic changes in the kidney that are independent of SBP. Atorvastatin corrected all, suggesting that the nitric oxide-oxidative stress balance plays a significant role in the earlier stages of salt induced kidney damage.

scholarly journals STUDIES ON EXPERIMENTAL HYPERTENSION

1943 ◽  
Vol 77 (4) ◽  
pp. 309-313 ◽  
Author(s):  
Harry Goldblatt ◽  
Yale J. Katz ◽  
Harvey A. Lewis ◽  
Evelyn Richardson
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Rapid Method ◽  
Standard Method ◽  
Renal Tissue ◽  
The Body ◽  
Experimental Hypertension

A simple, rapid method for the bioassay of renin has been presented. Reliable and consistent results are obtained by this method whereby an arbitrary dog unit of renin has been established. The response of normal unanesthetized dogs to renin is independent of the body weight of dogs weighing between 10 and 25 kilos. An estimate of potency of renin per kilo of body weight of the test animals is therefore not only unnecessary but misleading. A dog unit of renin has been defined as that amount which raises the blood pressure at least 30 and not more than 35 mm. Hg within 3 minutes in at least three unanesthetized dogs. The potency is expressed as dog units of renin per cubic centimeter. The determination of the amount of renal substance represented by a cubic centimeter of extract and the number of dog units per cubic centimeter give an estimate of the yield of renin which can be expressed as dog units of renin per gram of original renal tissue. By determination of the number of dog units per cubic centimeter and the amount of nitrogen in milligrams per cubic centimeter in any renal extract the purity of the renin can be determined and expressed as dog units of renin per milligram N. The establishment of a standard method for the bioassay of renin is considered highly desirable and the method outlined in this paper is suggested for this purpose.

High salt intake and blood pressure in lower primates (Papio hamadryas)

1976 ◽  
Vol 40 (4) ◽  
pp. 601-604 ◽  
Author(s):  
G. M. Cherchovich ◽  
K. Capek ◽  
Z. Jefremova ◽  
I. Pohlova ◽  
J. Jelinek
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Pulse Pressure ◽  
Renal Mass ◽  
Salt Intake ◽  
Control Level ◽  
Papio Hamadryas ◽  
Mean Blood Pressure ◽  
High Salt Intake ◽  
One Year

One year of increased salt intake in monkeys elevates mean blood pressure significantly. This effect is more marked in animals exposed just after birth. In animals exposed as adults, the response in males is more pronounced than in females, mainly due to a marked increase of pulse pressure. Th hypertensive response was potentiated by reduction of renal mass, which caused GFR values (in terms of body weight) to decrease compared with intact salt-fed animals, in which GFR values were elevated above the control level. It is concluded that the mechanisms involved in the hypertensive response are similar to those in the rat and dog.

Prevalence, Biochemical and Clinical Characteristics of Resistant Hypertension

2018 ◽  
Vol 69 (10) ◽  
pp. 2845-2849
Author(s):  
Daniela Gurgus ◽  
Elena Ardeleanu ◽  
Carmen Gadau ◽  
Roxana Folescu ◽  
Ioan Tilea ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Resistant Hypertension ◽  
Clinical Characteristics ◽  
Salt Intake ◽  
Target Organ Damage ◽  
Multivariate Logistic Regression Analysis ◽  
Organ Damage ◽  
Left Ventricular ◽  
High Salt Intake

The objectives of the present study were to evaluate the prevalence of resistant hypertension (RH) in primary care setting and to analyse its biochemical and clinical characteristics. After 3 months of treatment and evaluation, 721 (14.01%) of 5,146 patients with hypertension did not reach target office blood pressure of [ 140/90 mmHg. After exclusion of �white-coat effect� with ambulatory blood pressure, of secondary and pseudo- resistant hypertension, prevalence of RH was 6.74%. Lifestyle factors associated with RH were physical inactivity, obesity, high salt intake, smoking and excessive alcohol ingestion. Compared to controlled hypertension, RH patients presented higher incidence of family history of cardiovascular disease (38.90% vs 25.94%), diabetes mellitus (34.87% vs 19.01%), impaired fasting glucose (21.91% vs 19.07%), target organ damage (29.1% vs 15.95%), and cardiovascular disease (27.09% vs 17.06%). Dyslipidaemia (52.90% vs 42.03%), fasting plasma glucose (116.10�38.9 vs 107.80�37.2), HbA1c (6.41�1.42 vs 5.96�0.94), serum creatinine (1.09�0.27 vs 1.03�0.24) and microalbuminuria (21.90% vs 10.95%) were significantly higher in RH. Predictors of RH, determined by a multivariate logistic regression analysis were left ventricular hypertrophy (OD 2.14, 95% CI 1.32-3.69), renal impairment expressed as eGFR [ 60 ml/min/1.73m2 (OD 1.62, 95% CI 1.21-2.21) and the presence of cardiovascular disease (OD 1.48, 95% CI 1.02-2.16).

Blood Pressure and Intra-Erythrocyte Sodium during Normal and High Salt Intake in Middle-Aged Men: Relationship to Family History of Hypertension, and Neurogenic and Hormonal Variables

1984 ◽  
Vol 66 (4) ◽  
pp. 427-433 ◽  
Author(s):  
Ottar Gudmundsson ◽  
Hans Herlitz ◽  
Olof Jonsson ◽  
Thomas Hedner ◽  
Ove Andersson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Family History ◽  
Salt Intake ◽  
Sodium Intake ◽  
Positive Family History ◽  
Sodium Content ◽  
High Salt Intake ◽  
History Of ◽  
Family History Of Hypertension ◽  
Erythrocyte Sodium

1. During 4 weeks 37 normotensive 50-year-old men identified by screening in a random population sample were given 12 g of NaCl daily, in addition to their usual dietary sodium intake. Blood pressure, heart rate, weight, urinary excretion of sodium, potassium and catecholamines, plasma aldosterone and noradrenaline and intra-erythrocyte sodium content were determined on normal and increased salt intake. The subjects were divided into those with a positive family history of hypertension (n = 11) and those without such a history (n = 26). 2. Systolic blood pressure and weight increased significantly irrespective of a positive family history of hypertension. 3. On normal salt intake intra-erythrocyte sodium content was significantly higher in those with a positive family history of hypertension. During high salt intake intra-erythrocyte sodium content decreased significantly in that group and the difference between the hereditary subgroups was no longer significant. 4. In the whole group urinary excretion of noradrenaline, adrenaline and dopamine increased whereas plasma aldosterone decreased during the increased salt intake. 5. Thus, in contrast to some earlier studies performed in young subjects, our results indicate that moderately increased sodium intake acts as a pressor agent in normotensive middle-aged men whether there was a positive family history of hypertension or not. We confirm that men with positive family history of hypertension have an increased intra-erythrocyte sodium content, and that an increase in salt intake seems to increase overall sympathetic activity.

MO233RENAL ARTERY STENOSIS: DO NOT FORGET INHERITED THROMBOPHILIA

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Marwa Omrane ◽  
Yosra Ben Ariba ◽  
Imen Ouertani ◽  
Jannet Labidi
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Artery ◽  
High Blood Pressure ◽  
Protein C ◽  
Artery Bypass ◽  
Duplex Ultrasound ◽  
Protein S ◽  
Artery Stenosis ◽  
Inherited Thrombophilia

Abstract Background and Aims Inherited thrombophilia can be defined as a genetically determined predisposition to develop thromboembolic complications. Inherited prothrombotic risk factors include antithrombin deficiency, protein C and protein S deficiencies, activated protein C resistance due to Leiden factor V mutation, inherited hyperhomocysteinemia, prothrombin G20210A variant, dysfibrinogenemia and elevated factor VIII levels. Method We report the case of a patient with history of bilateral renal artery stenosis who presented with renal artery bypass thrombosis related to an inherited thrombophilia. Results We report a case of 40-year-old male patient who presented with extremely high blood pressure and hypokalemia without other biological abnormalities. The duplex ultrasound showed bilateral renal stenosis with chronic occlusion of the right renal artery and a tight stenosis of the left renal artery estimated at 50%. Renal angiography confirmed the bilateral stenosis, associated to a small right kidney. Renal scintigraphy with DMSA showed normal left renal function and right renal function estimated at 2%. The therapeutic decision was to perform an aorto-renal bypass surgery by the saphenous vein.After renal artery bypass the blood pressure improved markedly, maintaining this result at 12 months follow-up at clinical examination and duplex ultrasound. One year later, the patient presented with high blood pressure. The duplex ultrasound showed a stenosis of the bypass with a double stenosis of the left aorto renal bypass on renal angioscanner. The patient underwent angioplasty of the venous bridge with implantation of 2 stents with improvement of blood pressure after angioplasty. Six months later, the patient presented an unbalanced blood pressure, the ultrasound control with a vascular Doppler showed a stenosis at the stent. The antihypertensive treatment was increased, a thrombophilia balance was requested concluding a combined protein C and protein S deficiency. Conclusion An etiological assessment should be carried out systematically in the event of thrombosis occurring before the age of 40 or in the case of iterative venous or arterial thrombosis. A genetic study where appropriate and a family screening are then recommended.

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