Acute intracerebroventricular insulin microinjection after nitric oxide synthase inhibition of renal sodium handling in rats

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Objective: The current study considers changes of the postnatal brainstem cell number and angiotensin receptors by maternal protein restriction (LP) and LP taurine supplementation (LPT), and its impact on arterial hypertension development in adult life. Methods and results: The brain tissue studies were performed by immunoblotting, immunohistochemistry, and isotropic fractionator analysis. The current study shows that elevated blood pressure associated with decreased fractional urinary sodium excretion (FE Na ) in adult LP offspring was reverted by diet taurine supplementation. Also, that 12-day-old LP pups present a reduction of 21% of brainstem neuron counts, and, immunohistochemistry demonstrates a decreased expression of type 1 angiotensin II receptors (AT 1 R) in the entire medial solitary tract nuclei (nTS) of 16-week-old LP rats compared to age-matched NP and LPT offspring. Conversely, the immunostained type 2 AngII (AT 2 R) receptors in 16-week-old LP nTS were unchanged. Conclusion:The present investigation shows a decreased FE Na that occurs despite unchanged creatinine clearance. It is plausible to hypothesize an association of decreased postnatal nTS cell number, AT 1 R/AT 2 R ratio and FE Na with the higher blood pressure levels found in taurine-deficient progeny (LP) compared with age-matched NP and LPT offspring.

Section: Blood Pressure Measurementmentioning

confidence: 99%

Impact of taurine supplementation on blood pressure in gestational protein-restricted offspring: Effect on the medial solitary tract nucleus cell numbers, angiotensin receptors, and renal sodium handling

Scabora

Lima

Lopes

et al. 2013

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“…At the end of the experiment, blood samples were drawn through the tail vein or cardiac puncture in anaesthetised rats and urine and plasma samples were collected for analysis. [22][23][24] …”

Section: Renal Function Testmentioning

confidence: 99%

“…Creatinine clearance was used to estimate glomerular filtration rate (GFR) and lithium clearance (C Li ) was used to assess proximal tubule output. [21][22][23][24] Fractional sodium excretion (FE Na ) was calculated as C Na /C Cr × 100, where C Na is sodium clearance and C Cr is creatinine clearance. The fractional proximal (FEP Na ) and post-proximal (FEPP Na ) sodium excretion were calculated as C Li /C Cr × 100 and C Na /C Li × 100, respectively.…”

Section: Data Presentation and Statistical Analysismentioning

confidence: 99%

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

Ciampone

Borges

Lima

et al. 2011

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 agematched 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 (SHR T ) rats, compared with sedentary SHR (SHR S ), despite a significantly decreased creatinine clearance (C Cr ). Furthermore, immunoblotting analysis demonstrated a decreased expression of AT1 R in the entire kidney of T SHR rats, compared with S SHR . Conversely, the expression of the AT2 R , 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 T SHR rats compared with age-matched S SHR rats.

“…Fractional proximal (FEP Na ) and post-proximal (FEPP Na ) sodium excretion was calculated as C Li /C Cr × 100 and C Na /C Li × 100, respectively. [15][16][17] Data obtained over time were analysed using appropriate ANOVA for repetitive measurements. Post hoc comparisons between selected means were performed by Bonferroni's contrast test when initial ANOVA indicated statistical differences between experimental groups.…”

Section: Data Presentation and Statistical Analysismentioning

confidence: 99%

Impaired dipsogenic and renal response to repetitive intracerebroventricular angiotensin II (AngII) injections in rats

Zapparoli

Figueiredo

Bôer

et al. 2011

The role of the central nervous system (CNS) in the control of blood pressure and hydrosaline homeostasis has been demonstrated by several studies. While circulating angiotensin II (AngII) tends to retain sodium by a direct renal action as well as through aldosterone release, stimulation of brain AngII receptors has been reported to induce natriuresis. Repetitive intracerebroventricular AngII injection was recently demonstrated to be capable of leading to desensitisation of the dipsogenic effect of AngII stimuli. The aim of the current study was to investigate a possible central desensitisation to AngII stimuli by observing the effects of a low-concentration solution of AngII on the dipsogenic and natriuretic mechanisms in conscious rats, compared with appropriate age-matched 0.15 M NaCl-injected subjects, as evaluated by lithium clearance. The present report confirmed earlier reports on the potent natriuretic and dipsogenic effects of central AngII receptor stimulation. Natriuresis is mediated by a decrease in sodium reabsorption in the proximal and post-proximal tubule segments of the nephron. The current findings lend further support to the idea that AngII, in the CNS, is instrumental in the regulation of body fluid homeostasis. The magnitude of the dipsogenic and renal response to AngII was significantly decreased by repetitive stimulus.