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Biomedical subjects

G F DiBona

Publications and source records attributed to G F DiBona.

At least 19 recordsLinked to original sources
PubMed1996

Sex- and age-related antihypertensive effects of amlodipine. The Amlodipine Cardiovascular Community Trial Study Group.

This community-based study assessed whether there were age, sex, or racial differences in response to amlodipine 5 to 10 mg once daily in patients with mild to moderate essential hypertension. This prospective, open-label trial had a 2-week placebo period, a 4-week upward drug titration/efficacy period, and a 12-week drug maintenance period. There were 1,084 evaluable patients (mean age 55.5 years; 65% men and 35% women; 79% white and 21% black; 75% <65 and 25% > or = 65 years old). At the end of the titration/efficacy phase, the mean +/- SD blood pressure (BP) decreased by -16.3 +/- 12.3/-12.5 +/- 5.9 mm Hg, (p < or = 0.0001). Amlodipine produced a goal BP response (sitting diastolic BP < or = 90 mm Hg, or a 10 mm Hg decrease) in 86.0% of patients overall. The BP response was greater in women (91.4%) than in men (83.0%, p < or = 0.001), and greater in those > or = 65 years old (91.5%) than in those < 65 years old (84.1%, p < or = 0.01); however, it was similar between whites and blacks (86.0% vs 85.9%, respectively, p = NS). The sex difference in BP response could not be fully explained by differences in age, weight, dose (mg/kg), race, baseline BP, or compliance, and there were no differences among women based on use of hormone replacement therapy. Amlodipine was well tolerated; mild to moderate edema was the most common adverse effect. Thus, amlodipine was effective and safe as once-a-day monotherapy in the treatment of mild to moderate hypertension in a community-based population. Women had a greater BP response to amlodipine.

Adult↗
PubMed1996

Characteristics of renal sympathetic nerve activity in sodium-retaining disorders.

Characteristics of renal sympathetic nerve activity in conscious rats with established congestive heart failure, cirrhosis, or nephrotic syndrome were analyzed using three methods: mean integrated voltage over time, power spectrum analysis, and sympathetic peak detection analysis. Compared with control rats, all three disease models had increased mean integrated voltage. On power spectrum analysis, all three disease models had increased relative power at the heart rate frequency, indicating that it was related to renal sympathetic nerve discharge coupled to the cardiac cycle. Congestive heart failure and nephrotic syndrome rats showed increased relative power in the low-frequency range, whereas cirrhotic and nephrotic syndrome rats showed decreased relative power in the high-frequency range. On sympathetic peak detection analysis, the frequency of sympathetic peaks was greater in the three disease models compared with the control rats. In cirrhotic rats, the distribution of sympathetic peak heights was shifted toward an increased number of peaks of lesser height. It is concluded that basal renal sympathetic nerve activity is chronically increased in these disease models. This is manifest as increased power coupled to the cardiac cycle, which may reflect the disease-specific defects in arterial and cardiac baroreflex control. In cirrhosis, there is possible selective activation of a subgroup of renal sympathetic nerve fibers.

Animals↗
PubMed1996

Differentiated sympathetic neural control of the kidney.

Anatomic and neurophysiological methods were used to identify functionally specific subgroups of renal sympathetic nerve fibers. The distribution of diameters of the predominating unmyelinated fibers showed a major mode at 1.1 microns and a minor mode at 1.6 microns. The conduction velocity was 2.10 +/- 0.10 m/s, consistent with unmyelinated C fibers. Analysis of strength-duration relationships during renal nerve stimulation showed that both rheobase and chronaxie values for renal blood flow were greater than those for urinary flow rate and were independent of stimulation frequency. This difference suggests a higher stimulation threshold (smaller diameter) for those renal nerve fibers involved in the renal blood flow response (renal vasoconstriction) compared with those for the urinary flow rate response (antidiuresis) to renal nerve stimulation. Single renal units that responded to preganglionic splanchnic nerve stimulation were studied. Those with spontaneous activity (88%) responded to stimulation of arterial baroreceptors, arterial and central chemoreceptors, and peripheral thermoreceptors, whereas those that lacked spontaneous activity (12%) responded only to stimulation of peripheral thermoreceptors (known to produce renal vasoconstriction). A minority population of single renal units has been identified that, although renal vasoconstrictor, does not exhibit other characteristic features of vasoconstrictor neurons (i.e., responsiveness to stimulation of arterial baroreceptors and arterial and central chemoreceptors). These findings suggest the existence of functionally specific subgroups of renal nerve fibers.

Animals↗
PubMed1996

Effect of endogenous angiotensin II on renal nerve activity and its arterial baroreflex regulation.

To determine the effects of physiological alterations in endogenous angiotensin II (ANG II) activity on basal renal sympathetic nerve activity and its arterial baroreflex regulation, the effect of ANG II receptor (AT1) blockade with losartan was examined in conscious rats consuming low, normal, or high sodium diet that were instrumented for the simultaneous measurement of arterial pressure and renal sympathetic nerve activity. Intravenous losartan decreased arterial pressure in low (-27 +/- 4 mmHg) and normal (-15 +/- 2 mmHg) but not in high sodium diet rats (-5 +/- 2 mmHg). When arterial pressure had been restored to the prelosartan value with methoxamine infusion, renal sympathetic nerve activity was decreased in low (-27 +/- 4%) and normal (-20 +/- 3%) but not in high sodium diet rats (-5 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-8 +/- 2 mmHg) and normal (-7 +/- 2 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). Intracerebroventricular losartan did not significantly decrease arterial pressure but decreased renal sympathetic nerve activity in low (-28 +/- 5%) and normal (-20 +/- 4%) but not in high sodium diet rats (-2 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-7 +/- 2 mmHg) and normal (-5 +/- 1 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). These results indicate that physiological alterations in endogenous ANG II activity tonically influence basal levels of renal sympathetic nerve activity and its arterial baroreflex regulation.

Angiotensin II↗
PubMed1996

Acute sympathoinhibitory actions of metformin in spontaneously hypertensive rats.

Chronic treatment with the antihyperglycemic agent metformin prevents hypertension in spontaneously hypertensive rats. This effect has been ascribed to normalization of plasma insulin levels. However, whether metformin affects arterial pressure via changes in sympathetic nerve activity is unknown. Therefore, the objective of this study was to examine whether acute administration of metformin produces changes in mean arterial pressure, heart rate, or efferent renal sympathetic nerve activity in spontaneously hypertensive rats. Rats were anesthetized with alphaxalone-alphadolone (Saffan), paralyzed with pancuronium, and artificially ventilated. Intravenous administration of metformin (0, 1, 10, 100 mg/kg) produced dose-dependent reversible decreases in mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity that were not affected by arterial or cardiopulmonary baroreceptor denervation, nitric oxide synthase inhibition by N(omega)-nitro-L-arginine methyl ester, or cyclooxygenase inhibition by indomethacin. Metformin given into the lateral cerebral ventricle (250, 500, 1000 microg) produced dose-dependent decreases in mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity in doses that caused no changes when given intravenously. The sympathoinhibitory response to intracerebroventricular administration of metformin was not affected by alpha2-adrenoceptor blockade by intracerebroventricular yohimbine. We conclude that metformin has acute sympathoinhibitory effects (decreased arterial pressure, heart rate, and efferent renal sympathetic nerve activity) that are produced by a direct central nervous system site of action.

Animals↗
PubMed1996

Renal sympathetic neural mechanisms as intermediate phenotype in spontaneously hypertensive rats.

The borderline hypertensive rat, the F1 of a cross between a hypertensive spontaneously hypertensive rat (SHR) and a normotensive Wistar-Kyoto (WKY) rat, is a NaCl-sensitive model of genetic hypertension. In addition to hypertension, borderline hypertensive rats fed 8% NaCl develop characteristic alterations in the regulation of efferent renal sympathetic nerve activity and the neural control of renal function that are similar to those observed in the SHR parent. Like the normotensive WKY rat parent, borderline hypertensive rats fed 1% NaCl remain normotensive and do not exhibit these alterations in renal sympathetic neural mechanisms. These renal sympathetic neural mechanisms constitute a complex quantitative trait that may represent an intermediate phenotype. They have a plausible pathogenetic role in hypertension and are different between SHR and WKY rats. This study evaluated two aspects of this complex quantitative trait, enhanced renal sympathoexcitation with air-jet stress and enhanced renal sympathoinhibition with guanabenz, as a candidate intermediate phenotype. As neither of these aspects was observed in two-kidney, one clip Goldblatt-hypertensive rats, this suggests that the trait is not secondary to hypertension from an acquired cause. In a backcross population (F1 x WKY) fed 8% NaCl for 12 weeks, both enhanced renal sympathoexcitation with air-jet stress and enhanced renal sympathoinhibition with guanabenz cosegregated with the hypertension. These results support renal sympathetic neural mechanisms as an intermediate phenotype in SHR.

Animals↗
PubMed1995

Effect of amlodipine on left ventricular mass in the Amlodipine Cardiovascular Community Trial.

As part of the Amlodipine Cardiovascular Community Trial (ACCT), which was a large multicenter study designed to assess the effects of the calcium channel blocker amlodipine besylate (Norvasc) as monotherapy for treatment of mild to moderate hypertension, we sought to determine the effects of amlodipine on regression of left ventricular (LV) hypertrophy (LVH). The study began with a 2-week placebo run-in period (baseline), before which antihypertensive drugs had been discontinued. Amlodipine was then administered at 5-10 mg/day during a 4-week titration/efficacy period. Patients achieving a goal diastolic blood pressure (DBP) of < or = 90 mm Hg or a decrease in DBP of > or = 10 mm Hg entered a 12-week maintenance phase and had the option to continue long-term therapy thereafter. Echocardiograms were obtained in a subset of patients at the end of the baseline period. In patients with LVH at baseline, echocardiograms were repeated at the end of 16 weeks of therapy (week 18), and at 42 weeks in patients continuing long-term therapy. Thirty-seven percent of 124 hypertensive patients screened for LVH at baseline had LVH detected on echocardiograms. Blacks had a higher incidence of LVH (64%) as compared with whites (34%, p < 0.05). Patients with LVH were more likely to have a higher baseline systolic BP (SBP) and DBP. Their sitting SBP and DBP decreased significantly from a mean of 163/102 mm Hg at baseline to 139/86 mm Hg with amlodipine therapy at week 18 (p < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Furosemide elicits immediate sympathoexcitation via a renal mechanism independent of angiotensin II.

This investigation aimed at examing the hypothesis that furosemide elicits renal sympathoexcitation through stimulation of renal renin release, which in turn produces increased plasma angiotensin II levels, causing centrally mediated sympathoexcitation. In addition, direct central nervous actions of furosemide on central control of mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity were examined. Furosemide (300 mg/kg intravenously) was administered to four groups of rats: (1) control; (2) nephrectomized; (3) with intravenous losartan blockade (10 mumol/kg); and (4) with intracerebroventricular losartan blockade (10 nmol). In a fifth group of rats, furosemide was administered intracerebroventricularly (0, 2.5, 25 or 250 micrograms). To eliminate reflex control of mean arterial pressure, heart rate and efferent renal sympathetic nerve activity, all experiments were performed in rats with sinoaortic denervation and bilateral vagotomy. Experiments were performed during Saffan anaesthesia (0.9% alphaxalone/0.3% alphadolone), and rats were paralyzed with pancuronium and artifically ventilated. Furosemide produced an immediate 40% increase in efferent renal sympathetic nerve activity while the furosemide vehicle, 2 vol.% ethanolamine, did not affect efferent renal sympathetic nerve activity. The furosemide-induced increase in efferent renal sympathetic nerve activity was abolished in rats with bilateral nephrectomy but it was not affected by intravenous or intracerebroventricular losartan blockade. Intracerebroventricular angiotensin II produced an increase in mean arterial pressure and efferent renal sympathetic nerve activity whereas intravenous angiotensin II produced a pressor response in absence of increased efferent renal sympathetic nerve activity. Losartan effectively blocked responses to intravenous or intracerebroventricular angiotensin II. Intracerebroventricular administration of furosemide produced no changes in mean arterial pressure, heart rate or efferent renal sympathetic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1995

Hepatorenal baroreflex in cirrhotic rats.

A hepatorenal baroreflex has been described in which increases in intrahepatic sinusoidal pressure stimulate an intrahepatic baroreceptor, resulting in increases in afferent hepatic (HNA) and efferent renal sympathetic nerve activity (RNA). Hepatic denervation prevents the increase in RNA. This baroreflex is postulated to contribute to the increase in RNA found in cirrhosis in which intrahepatic sinusoidal pressure is increased. However, the increased fibrosis in the cirrhotic liver may render the intrahepatic baroreceptor less sensitive to increases in intrahepatic sinusoidal pressure. By use of thoracic inferior vena caval constriction, intrahepatic sinusoidal pressure (i.e., inferior vena caval pressure, IVCP) was increased in control rats and rats with cirrhosis due to common bile duct ligation (CBDL) while HNA and RNA were measured. With increases in IVCP of 5 mmHg, increases in HNA (+38 +/- 2 and +44 +/- 3%) and RNA (+25 +/- 1 and +34 +/- 3%) were not different in control and CBDL rats, respectively. The slope gain, % delta HNA/delta IVCP, was +7.1 +/- 0.6 and +8.1 +/- 0.7%/mmHg in control and CBDL rats, respectively. Therefore the hepatorenal baroreflex is not desensitized in the CBDL rat, and the hepatorenal baroreflex is capable of contributing to the increase in RNA observed in cirrhosis.

Afferent Pathways↗
PubMed1995

Increased renal nerve activity in cardiac failure: arterial vs. cardiac baroreflex impairment.

Cardiac failure is characterized by increased renal sympathetic nerve activity that is associated with an impairment of both arterial and cardiac baroreceptor reflex function. These reflex dysfunctions are in the afferent limb at the level of the peripheral baroreceptors. This study sought to define the relative quantitative magnitude of the defects in arterial and cardiac baroreceptor function in cardiac failure. Renal sympathetic nerve activity was measured in anesthetized normal control rats and rats with cardiac failure (left coronary ligation) during sequential random order sinoaortic denervation and vagotomy to interrupt afferent input from the arterial and cardiac baroreceptors, respectively. Increases in renal sympathetic nerve activity after individual or combined sinoaortic denervation and vagotomy were less (P < 0.05 for both) in cardiac failure than in normal control rats in both order sequences (42 +/- 5 vs. 87 +/- 8%; 44 +/- 5 vs. 108 +/- 7%). In cardiac failure rats, vagotomy produced lesser increases (P < 0.05 for both) in renal sympathetic nerve activity than sinoaortic denervation in both order sequences (10 +/- 4 vs. 32 +/- 5%; 13 +/- 2 vs. 30 +/- 5%). The relative magnitude of impaired cardiac baroreceptor reflex function that is associated with the increased renal sympathetic nerve activity of cardiac failure is greater than that of impaired arterial baroreceptor reflex function.

Analysis of Variance↗
PubMed1995

Arterial and cardiopulmonary baroreflex control of renal nerve activity in cirrhosis.

Cirrhotic rats (common bile duct ligation; CBDL) have increased efferent renal sympathetic nerve activity (ERSNA), which contributes significantly to the observed renal sodium and water retention and edema formation. Basal ERSNA is increased and fails to suppress normally during intravenous isotonic saline volume expansion. Arterial and cardiopulmonary baroreflex control of ERSNA in CBDL and control (CTR) rats was examined. CBDL rats exhibited hyperdynamic circulation with increased cardiac index and decreased total peripheral resistance index and arterial pressure compared with CTR rats. Increases in left ventricular end-diastolic pressure (LVEDP) produced by volume expansion increased cardiac index normally in CBDL rats. The maximal gain of aortic baroreflex control of ERSNA was similar in CBDL and CTR rats. In CBDL rats, during decreased arterial pressure, there was a decreased range of the central component, which accounted for the decreased range of the overall aortic baroreflex, with the range of the afferent component being normal. For cardiopulmonary baroreflex control of ERSNA, the LVEDP threshold was increased and the gain was decreased in CBDL compared with CTR rats; this was due to an increased LVEDP threshold and a diminished gain of the afferent component while the central portion of the reflex was normal. These abnormalities in the cardiopulmonary baroreflex account for the attenuated decrease in ERSNA in CBDL compared with CTR rats during volume expansion. In CBDL rats, attenuation of cardiopulmonary baroreflex control of ERSNA contributes to both the increased basal ERSNA and its failure to normally suppress during volume expansion.

Analysis of Variance↗
PubMed1995

ANG II receptor blockade and arterial baroreflex regulation of renal nerve activity in cardiac failure.

In cardiac failure, efferent renal sympathetic nerve activity (ERSNA) and the activity of the renin-angiotensin system are increased, and arterial baroreflex regulation of ERSNA is attenuated. We examined the effect of intravenous and intracerebroventricular angiotensin II AT receptor blockade with losartan on the arterial baroreflex regulation of ERSNA in conscious control (C) and congestive heart failure (CHF) rats. Intravenous losartan (10 mg/kg, 21.7 mumol/kg) decreased arterial pressure more in CHF than in C rats (-28 +/- 3 vs. -20 +/- 3 mmHg, P < 0.05). After restoration of arterial pressure to the prelosartan value with methoxamine infusion, ERSNA was decreased more in CHF than in C rats (-23 +/- 4 vs. -1 +/- 2%, P < 0.05). Maximal gain of arterial baroreflex control of ERSNA (Gmax) was lower in CHF compared with C rats (-1.94 +/- 0.10 vs. -3.78 +/- 0.21%/mmHg, P < 0.05). Intravenous losartan increased Gmax in CHF (to -3.01 +/- 0.14%/mmHg, P < 0.05) but not in C rats (to -3.56 +/- 0.19%/mmHg). Intracerebroventricular losartan (4.61 micrograms, 10 nmol) did not affect arterial pressure but decreased ERSNA more in CHF than in C rats (-13 +/- 2 vs. -8 +/- 3%, P < 0.05). Like intravenous losartan, intracerebroventricular losartan increased Gmax in CHF (from -2.11 +/- 0.18 to -3.21 +/- 0.30%/mmHg, P < 0.05) but not in C rats (from -3.98 +/- 0.25 to -3.84 +/- 0.22%/mmHg). These results suggest that increased activity of the renin-angiotensin system contributes to the increase in ERSNA and its abnormal arterial baroreflex regulation in cardiac failure.

Angiotensin Receptor Antagonists↗
PubMed1995

Analysis of renal sympathetic nerve responses to stress.

We studied sympathetic nerve activity responses to acute environmental stress (air jet stress) in conscious Wistar-Kyoto, spontaneously hypertensive, and borderline hypertensive rats. The borderline hypertensive rats were fed either 1% (normotensive) or 8% (hypertensive) NaCl. Renal sympathetic nerve activity responses were analyzed with three methods: mean integrated voltage over time, power spectrum analysis, and sympathetic peak detection analysis. Measurements of mean integrated voltage over time showed that air jet stress increased renal sympathetic nerve activity in spontaneously hypertensive rats and in borderline hypertensive rats on 8% NaCl but not in the other groups. In the NaCl responders, power spectrum analysis of renal sympathetic nerve activity indicated that the increase in relative power was at the heart rate frequency, indicating that it was related to renal sympathetic nerve discharge coupled to the cardiac cycle. Sympathetic peak detection analysis of renal sympathetic nerve activity indicate that there was an increase in frequency of sympathetic peaks of greater height and shorter duration because of sinoaortic baroreceptor deactivation (increased peak frequency) and the recruitment of more active fibers (greater peak height) firing with greater synchronization (shorter peak duration). Additional methods of analysis of renal sympathetic nerve activity provide information in addition to that derived from measurement of mean integrated voltage over time.

Animals↗
PubMed1995

Cardiopulmonary baroreflex function in nephrotic rats.

Efferent renal sympathetic nerve activity is increased in experimental nephrotic syndrome and exhibits attenuated cardiopulmonary baroreflex inhibition during volume expansion in anesthetized rats. Additional studies were performed in conscious rats to avoid the potentially confounding influences of anesthesia; these studies used another more specific standardized stimulus for cardiopulmonary baroreflex activation. Sprague Dawley rats were studied 3 to 4 wk after adriamycin injection (3.5 mg/kg iv); all rats developed proteinuria. In sinoaortic denervated rats (anesthetized), graded frequency stimulation of the central end of the cut right vagus nerve produced frequency-dependent decreases in mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity. The decreases in mean arterial pressure and heart rate were similar in control and nephrotic rats, but efferent renal sympathetic nerve activity decreased significantly less in nephrotic than control rats over the entire frequency range (P < 0.02). In sinoaortic denervated rats (conscious), 10% body weight isotonic saline volume expansion decreased mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity. The decreases in mean arterial pressure and heart rate were similar in control and nephrotic rats, but efferent renal sympathetic nerve activity decreased significantly less in nephrotic than control rats over the entire period of volume expansion (P < 0.04). In nephrotic syndrome, the cardiopulmonary baroreflex inhibition of efferent renal sympathetic nerve activity is decreased; the defect lies in the central portion of the reflex. This may contribute to the observed increase in efferent renal sympathetic nerve activity in nephrotic syndrome.

Animals↗
PubMed1995

Renal neural mechanisms in salt-sensitive hypertension.

Genetic forms of salt (NaCl)-sensitive hypertension are characterized by increased renal sympathetic nerve activity responses to environmental stimuli. The increases in renal sympathetic nerve activity produce marked changes in renal function with renal vasoconstriction and sodium and water retention which can contribute to the initiation, development and maintenance of hypertension. In genetic forms of NaCl-sensitive hypertension, increased dietary NaCl intake produces alterations in norepinephrine kinetics with decreased concentrations of norepinephrine in regions of the anterior hypothalamus which are critical for the regulation of peripheral sympathetic nerve activity. This local central decrease in tonic alpha 2 adrenoceptor sympathoinhibitory input leads to increased peripheral (renal) sympathetic nerve activity and hypertension. Similarly, with increased dietary NaCl intake, patients with NaCl-sensitive hypertension develop increased arterial pressure, renal vasoconstriction, increased glomerular capillary pressure and increased urinary albumin excretion. Thus, increased dietary NaCl intake can, via central nervous system actions, produce increases in renal sympathetic nerve activity whose renal functional effects contribute to the pathophysiology of hypertension.

Animals↗
PubMed1995

Acute environmental stress overrides cardiac volume receptor reflex in borderline hypertensive rats.

OBJECTIVE: To examine whether acute environmental stress (air-jet stress) modulates the exaggerated natriuresis to volume expansion in conscious borderline hypertensive rats. DESIGN: Intravenous isotonic saline volume expansion was performed with and without superimposed acute air-jet stress in conscious borderline hypertensive rats which had consumed a 1% NaCl diet (normotensive) or an 8% NaCl diet (hypertensive) for 12 weeks. METHODS: Conscious rats were instrumented for measurement of arterial pressure, renal sympathetic nerve activity and collection of bladder urine. RESULTS: Arterial pressure was greater in the 8% NaCl borderline hypertensive rats than in the 1% NaCl borderline hypertensive rats. In the absence of acute air-jet stress the 8% NaCl borderline hypertensive rats exhibited exaggerated natriuresis and exaggerated inhibition of renal sympathetic nerve activity compared with the 1% NaCl borderline hypertensive rats. Acute air-jet stress increased both arterial pressure and renal sympathetic nerve activity reversibly, and attenuated natriuresis in the 8% NaCl but not in the 1% NaCl borderline hypertensive rats. CONCLUSION: Acute environmental stress (air-jet stress) attenuates exaggerated natriuresis in hypertensive but not in normotensive borderline hypertensive rats via increased renal sympathetic nerve activity.

Acute Disease↗
PubMed1994

Neural control of renal function in health and disease.

The renal sympathetic innervation of the kidney exerts significant effects on multiple aspects of renal function, including renal haemodynamics, tubular sodium and water reabsorption and renin secretion. These effects constitute an important control system which is important in the physiological regulation of arterial pressure and total body fluid and sodium homeostasis. Abnormalities in this regulatory mechanism have pathophysiological consequences and are manifest in clinically relevant human disease states. Decreased renal sympathetic nerve activity results in impaired renin secretion, the inability to conserve sodium normally and an attenuated ability to dispose of both acute and chronic sodium loads. Increased renal sympathetic nerve activity contributes significantly to the excess renal sodium retention and related renal abnormalities observed in both hypertension and oedema forming conditions, such as cardiac failure, cirrhosis and nephrotic syndrome.

Animals↗