scholarly journals IGF-1 deletion affects renal sympathetic nerve activity, left ventricular dysfunction, and renal function in DOCA-salt hypertensive mice

2019 ◽  
pp. 209-217
Author(s):  
Bing Xiao ◽  
Fan Liu ◽  
Jing-Chao Lu ◽  
Fei Chen ◽  
Wei-Na Pei ◽  
...  
Keyword(s):  
Renal Function ◽  
Left Ventricular Dysfunction ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Nerve Activity ◽  
Urea Nitrogen ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

The objective of the paper is to determine the influence of IGF-1 deletion on renal sympathetic nerve activity (RSNA), left ventricular dysfunction, and renal function in deoxycorticosterone acetate (DOCA)-salt hypertensive mice. The DOCA-salt hypertensive mice models were constructed and the experiment was classified into WT (Wild-type mice) +sham, LID (Liverspecific IGF-1 deficient mice) + sham, WT + DOCA, and LID + DOCA groups. Enzyme-linked immunosorbent assay (ELISA) was used to detect the serum IGF-1 levels in mice. The plasma norepinephrine (NE), urine protein, urea nitrogen and creatinine, as well as RSNA were measured. Echocardiography was performed to assess left ventricular dysfunction, and HE staining to observe the pathological changes in renal tissue of mice. DOCA-salt induction time-dependently increased the systolic blood pressure (SBP) of mice, especially in DOCA-salt LID mice. Besides, the serum IGF-1 levels in WT mice were decreased after DOCA-salt induction. In addition, the plasma NE concentration and NE spillover, urinary protein, urea nitrogen, creatinine and RSNA were remarkably elevated with severe left ventricular dysfunction, but the creatinine clearance was reduced in DOCA-salt mice, and these similar changes were obvious in DOCA-salt mice with IGF-1 deletion. Moreover, the DOCA-salt mice had tubular ectasia, glomerular fibrosis, interstitial cell infiltration, and increased arterial wall thickness, and the DOCA-salt LID mice were more serious in those aspects. Deletion of IGF-1 may lead to enhanced RSNA in DOCA-salt hypertensive mice, thereby further aggravating left ventricular dysfunction and renal damage.

Increased renal sympathetic nerve activity leads to hypertension and renal dysfunction in offspring from diabetic mothers

2013 ◽  
Vol 304 (2) ◽  
pp. F189-F197 ◽  
Author(s):  
Aline Fernanda de Almeida Chaves Rodrigues ◽  
Ingrid Lauren Brites de Lima ◽  
Cássia Toledo Bergamaschi ◽  
Ruy Ribeiro Campos ◽  
Aparecida Emiko Hirata ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Dysfunction ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renal Nerves ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Diabetic Mothers ◽  
Renal Sympathetic

The exposure of the fetus to a hyperglycemic environment promotes the development of hypertension and renal dysfunction in the offspring at adult age. We evaluated the role of renal nerves in the hypertension and renal changes seen in offspring of diabetic rats. Diabetes was induced in female Wistar rats (streptozotocin, 60 mg/kg ip) before mating. Male offspring from control and diabetic dams were studied at an age of 3 mo. Systolic blood pressure measured by tail cuff was increased in offspring of diabetic dams (146 ± 1.6 mmHg, n = 19, compared with 117 ± 1.4 mmHg, n = 18, in controls). Renal function, baseline renal sympathetic nerve activity (rSNA), and arterial baroreceptor control of rSNA were analyzed in anesthetized animals. Glomerular filtration rate, fractional sodium excretion, and urine flow were significantly reduced in offspring of diabetic dams. Two weeks after renal denervation, blood pressure and renal function in offspring from diabetic dams were similar to control, suggesting that renal nerves contribute to sodium retention in offspring from diabetic dams. Moreover, basal rSNA was increased in offspring from diabetic dams, and baroreceptor control of rSNA was impaired, with blunted responses to infusion of nitroprusside and phenylephrine. Thus, data from this study indicate that in offspring from diabetic mothers, renal nerves have a clear role in the etiology of hypertension; however, other factors may also contribute to this condition.

Neural control of renal function

1997 ◽  
Vol 77 (1) ◽  
pp. 75-197 ◽  
Author(s):  
G. F. DiBona ◽  
U. C. Kopp
Keyword(s):  
Renal Function ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Renal Nerves ◽  
Communication Link ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Functional Components ◽  
Renal Sympathetic

The renal nerves are the communication link between the central nervous system and the kidney. In response to multiple peripheral and central inputs, efferent renal sympathetic nerve activity is altered so as to convey information to the major structural and functional components of the kidney, the vessels, glomeruli, and tubules, each of which is innervated. At the level of each of these individual components, information transfer occurs via interaction of the neurotransmitter released at the sympathetic nerve terminal-neuroeffector junction with specific postjunctional receptors coupled to defined intracellular signaling and effector systems. In response to normal physiological stimuli, changes in efferent renal sympathetic nerve activity contribute importantly to homeostatic regulation of renal blood flow, glomerular filtration rate, renal tubular epithelial cell solute and water transport, and hormonal release. Afferent input from sensory receptors located in the kidney participates in this reflex control system via renorenal reflexes that enable total renal function to be self-regulated and balanced between the two kidneys. In pathophysiological conditions, abnormal regulation of efferent renal sympathetic nerve activity contributes significantly to the associated abnormalities of renal function which, in turn, are of importance in the pathogenesis of the disease.

Effects of volume expansion on renal sympathetic nerve activity and cardiovascular and renal function in lambs

1992 ◽  
Vol 262 (4) ◽  
pp. R651-R658 ◽  
Author(s):  
F. G. Smith ◽  
J. M. Klinkefus ◽  
J. E. Robillard
Keyword(s):  
Renal Function ◽  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Right Atrial ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Cardiopulmonary Baroreflex ◽  
Renal Sympathetic

To assess the cardiopulmonary baroreflex in the immature animal, effects of volume expansion on changes in right atrial pressure, renal sympathetic nerve activity, and renal function were measured in chronically instrumented newborn (4-8 days; n = 13) and older lambs (4-5 wk; n = 14). Studies were carried out for 30 min before and 2 h after volume expansion with 6% Dextran 70 (25 ml/kg). Right atrial pressure increased by 4.0 +/- 0.5 mmHg in newborns and by 8.8 +/- 0.6 mmHg in older lambs within 15 min of volume expansion (P less than 0.001). After volume expansion, heart rate decreased in newborns from 237 +/- 6 beats/min to a nadir of 211 +/- 7 beats/min 2 h later (P less than 0.001) but remained constant at control levels of 148 +/- 9 beats/min in older lambs. Maximal inhibition of renal sympathetic nerve activity was achieved at 15 min in older lambs (-50.1 +/- 7.5%) and at 60 min (-58.3 +/- 10.9%) in newborns in which there was a prolonged sympathoinhibition (P less than 0.001). There was also a significant diuretic response in both groups but a limited natriuretic response to volume expansion in newborns (P greater than 0.05) compared with older lambs (P less than 0.001). These data demonstrate the presence of the cardiopulmonary baroreflex in the first week of life in lambs. The sustained sympathoinhibition and bradycardia seen in response to volume expansion in newborns but not in older lambs support the hypothesis that the reflexes controlling arterial pressure and blood volume change with postnatal maturation.

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