scholarly journals Effects of dopamine on urinary sodium excretion in spontaneously hypertensive rats

1989 ◽  
Vol 30 (4) ◽  
pp. 593-593
Author(s):  
Yoko Jo ◽  
Takuzo Hano ◽  
Hideki Nishio ◽  
Kenji Ueshima ◽  
Masahiko Shiotani ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Renal Function and Sympathetic Activity during Mental Stress in Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 327s-330s ◽  
Author(s):  
S. Lundin ◽  
P. Thorén
Keyword(s):  
Sodium Excretion ◽  
Sympathetic Activity ◽  
Mental Stress ◽  
Spontaneously Hypertensive Rats ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Renal Sympathetic

1. The role of the renal sympathetic nerves in the urinary sodium excretion response to ‘mental stress’ in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto normotensive (WKY) rats was examined. Urinary sodium excretion was measured during ‘rest’ and during a 20 min period of ‘mental stress’ in intact rats and in renal denervated rats. Under similar conditions renal sympathetic activity was also measured in a separate group of rats. 2. Urinary sodium excretion fell more during the stress period in SHR (-64 ± 5%) than in WKY rats (-34 ± 7%), despite a greater arterial pressure increase in SHR. This greater decrease in sodium excretion appeared to result from both a more pronounced reduction in GFR and a greater increase in tubular sodium reabsorbtion. 3. Renal sympathetic nerve activity, which was higher at rest in SHR than in WKY rats, increased much more in SHR than in WKY rats during stress. This may explain the greater reduction in sodium excretion in SHR during stress, because renal denervation almost abolished this latter response. 4. The neurogenically elicited renal response might contribute in an important way to the early development of SHR hypertension. Renal denervation, as well as attenuating sodium retention, also delays the pressure rise in the young SHR. 5. The initial tachycardia after mental stress gradually subsided towards the end of the stress period in SHR, whereas renal sympathetic activity remained elevated. This indicates that the increase in heart rate, if anything, may underestimate the true extent of sympathetic activation in for example the renal and splanchnic regions during arousal.

Stimulating effects of atenolol on vasodepressor prostaglandin generation in spontaneously hypertensive rats

1991 ◽  
Vol 81 (s25) ◽  
pp. 499-507 ◽  
Author(s):  
Nobuhito Hirawa ◽  
Yoshio Uehara ◽  
Atsushi Numabe ◽  
Satoru Takada ◽  
Hiroaki Matsuoka ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Blood Pressure Reduction ◽  
Vascular Wall ◽  
Urinary Sodium Excretion ◽  
Prostaglandin Synthesis ◽  
Dependent Manner ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

1. To assess the role of the vasodepressor prostaglandin system in the antihypertensive properties of β-adrenoceptor antagonist, we investigated the alterations of prostaglandin generation in the kidney and in the aorta when spontaneously hypertensive rats were treated with atenolol for 2 weeks. 2. The blood pressure reduction was associated with an increase in urinary sodium excretion and urinary prostaglandin E2 excretion. The sodium excretion was positively related to the prostaglandin E2 excretion. 3. Basal release of prostaglandin E2 from the sliced renal cortex was enhanced by the atenolol treatment. Prostacyclin-generating capacity in the aortic wall was also significantly increased. 4. Atenolol treatment stimulated prostaglandin synthesis in the kidney and vascular wall in a dose-dependent manner. However, atenolol per se did not directly stimulate prostaglandin synthesis in the vascular wall. 5. Inhibition of prostaglandin generation by a cyclo-oxygenase inhibitor, indomethacin, was associated with attenuation of the antihypertensive effects of atenolol. 6. Thus these data indicate that sub-chronic atenolol treatment stimulates vasodepressor prostaglandin generation in the kidney and in the aortic vessels, and this shares the antihypertensive effects of this drug with the mechanism of β-adrenergic antagonism probably mediated through vasorelaxation and natriuresis.

Aggravation of Hypertension in Spontaneously Hypertensive Rats by Heymann Nephritis

1981 ◽  
Vol 60 (3) ◽  
pp. 267-272 ◽  
Author(s):  
I. Tikkanen ◽  
A. Miettinen ◽  
F. Fyhrquist ◽  
T. Törnroth
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Spontaneously Hypertensive Rats ◽  
Rat Kidney ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Hypertensive Rats ◽  
New Approach ◽  
Spontaneously Hypertensive ◽  
Heymann Nephritis

1. To explore the effect of nephritis on development of genetic hypertension we immunized 10-week-old spontaneously hypertensive rats with purified rat kidney brush-border antigen. This induces Heymann nephritis (autologous immune complex nephritis), which does not elevate blood pressure in normal rats. 2. Nephritis developed in 11 of the 12 immunized animals, and systolic blood pressure rose to a significantly higher level than in the non-immunized spontaneously hypertensive rats within 4 weeks. Blood pressure remained higher in the immunized rats at 17 weeks, heart weights were greater, but creatinine clearance remained unchanged. 3. At 6 weeks, urinary sodium excretion was greater in the immunized spontaneously hypertensive rats, whereas at 17 weeks, sodium excretion was decreased in these animals along with reduced serum protein concentration, packed cell volume and plasma renin activity, as compared with that of the controls. 4. Development of hypertension in nephritic rats, therefore, appeared unrelated to sodium excretion; signs of volume expansion emerged later. 5. Acceleration of the development of spontaneous hypertension by Heymann nephritis, also leading to sustained higher blood pressure levels than in spontaneously hypertensive rats, offers a new approach to experimental study of immune mechanisms behind acceleration of pre-existing hypertension. This may have important bearings on essential hypertension as well.

scholarly journals Long-term exercise attenuates blood pressure responsiveness and modulates kidney angiotensin II signalling and urinary sodium excretion in SHR

2011 ◽  
Vol 12 (4) ◽  
pp. 394-403 ◽  
Author(s):  
Silmara Ciampone ◽  
Rafael Borges ◽  
Ize P de Lima ◽  
Flávia F Mesquita ◽  
Elizabeth C Cambiucci ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Exercise Training ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Receptor Expression ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Observations have been made regarding the effects of long-term exercise training on blood pressure, renal sodium handling and renal renin–angiotensin–aldosterone (RAS) intracellular pathways in conscious, trained Okamoto–Aoki spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKy) normotensive rats, compared with appropriate age-matched sedentary SHR and WKy. To evaluate the influence of exercise training on renal function and RAS, receptors and intracellular angiotensin II (AngII) pathway compounds were used respectively, and lithium clearance and western blot methods were utilised. The current study demonstrated that increased blood pressure in SHR was blunted and significantly reduced by long-term swim training between the ages of 6 and 16 weeks. Additionally, the investigators observed an increased fractional urinary sodium excretion in trained SHR (SHRT) rats, compared with sedentary SHR (SHRS), despite a significantly decreased creatinine clearance (CCr). Furthermore, immunoblotting analysis demonstrated a decreased expression of AT1R in the entire kidney of TSHR rats, compared with SSHR. Conversely, the expression of the AT2R, in both sedentary and trained SHR, was unchanged. The present study may indicate that, in the kidney, long-term exercise exerts a modulating effect on AngII receptor expression. In fact, the present study indicates an association of increasing natriuresis, reciprocal changes in renal AngII receptors and intracellular pathway proteins with the fall in blood pressure levels observed in TSHR rats compared with age-matched SSHR rats.

Aldosterone in the exaggerated natriuresis of spontaneously hypertensive rats

1978 ◽  
Vol 234 (1) ◽  
pp. F29-F35 ◽  
Author(s):  
L. R. Willis ◽  
J. H. Bauer
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Hypertensive Rats ◽  
Plasma Aldosterone Concentration ◽  
Salt Loading ◽  
Spontaneously Hypertensive ◽  
Salt Load ◽  
Total Body

The effect of mineralocorticoid hormones on the urinary responses of spontaneously hypertensive and normotensive rats to oral salt loading was determined. In response to a control salt load, the increase was determined. In response to a control salt load, the increase in urinary sodium excretion by the spontaneously hypertensive rats was significantly greater than that of the normotensive rats [48 +/- 6 (SE) mueq/h vs. 26 +/- 4 mueq/h]. Treatment with spironolactone did not significantly alter the natriuretic response of the spontaneously hypertensive rats (43 +/- 8 mueq/h) to another salt load, but increased the natriuretic response of the normotensive rats (55 +/- 7 mueq/h) to that of the hypertensive rats. D-Aldosterone suppressed the natriuretic response to salt loading of the hypertensive rats to a level which was not significantly different from that of the normotensive rats. Plasma aldosterone concentration was significantly lower in the spontaneously hypertensive rats than in the normotensive rats (18.0 +/- 3.3 and 52.1 +/- 5.2 ng/100 ml, respectively). Neither extracellular fluid volume nor total body water in spontaneously hypertensive and normotensive rats were significantly different. The data support the hypothesis that the exaggerated natriuresis in the spontaneously hypertensive rats is mediated by a relative lack by these rats of aldosterone-mediated distal tubular sodium reabsorption.

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