Behavioural stress blunts the creatinine clearance increase induced by a protein load in healthy subjects.

BACKGROUND: The aim of this study was to investigate how behavioural states related to different levels of stress affected the increments of glomerular filtration rate induced by an acute protein load. METHODS: Thirteen healthy subjects were enrolled. Each subject was studied from 9:00 h to 15:00 h on two consecutive days. In random order, after a protein meal (1.2 g/kg b.w. of protein), each subject was required to remain in a relaxing, sitting position (resting period, R), or to solve graphical and mathematical problems (behavioural stress period, S). Mean blood pressure (MBP) and heart rate (HR) were monitored by an ambulatory blood pressure device. Urine samples collected in each period were used to measure glomerular filtration rate (GFR, creatinine clearance) and urinary sodium excretion (UNa+V). RESULTS: Significant decreases in MBP and HR were observed during the resting period after the protein load, which significantly increased GFR. There was also a large increase of UNa+V. During S, the GFR changes were no longer seen whereas the increse of UNa+V was maintained. HR and MBP did not change compared to the prestimulus period. CONCLUSIONS: We conclude that in healthy subjects behavioural stress can blunt the increase in GFR that follows a protein load, presumably by neuro-humoral activated mechanisms. In our experimental conditions, behavioural stress did not affect UNa+V.

Short-term analysis of the relationship between blood pressure and urinary sodium excretion in normotensive subjects.

The aim of this study was to investigate whether, in the short term, physiological blood pressure changes are coupled with changes in urinary sodium excretion in normotensive subjects, maintained at fixed sodium intake and under controlled postural and behavioural conditions. Twelve normotensive subjects were recruited. For each subject, seven urine samples were collected at fixed time intervals during an overall 26 h period: late afternoon (16.00-20.00 hours), evening (20.00-24.00 hours), night (24.00-06.00 hours), quiet wakefulness (06.00-09.00 hours), morning (09.00-12.00 hours), post-prandial (12.00-15.00 hours) and afternoon (15.00-18.00 hours). Blood pressure was monitored by an ambulatory blood pressure device during the whole 26 h period. Each urine sample was used to measure urinary sodium excretion and glomerular filtration rate (creatinine clearance). Blood pressure, heart rate, urinary sodium excretion and glomerular filtration rate recorded in the daytime were higher than those measured during the night-time. A significant positive correlation between mean blood pressure and urinary sodium excretion was found during the night, over the whole 26 h period, and during two subperiods of the daytime: quiet wakefulness and the post-prandial period. The coefficient of the pressure-natriuresis curve was significantly decreased by postural changes. We conclude that, in normotensive subjects, blood pressure and urinary sodium excretion are coupled in the short term. The assumption of an upright posture can mask this relationship, presumably by activating neurohumoral factors.

Electrophysiological evidence of ipsilateral reno-renal reflexes in the cat.

To verify the existence of ipsilateral reno-renal reflexes we studied the effect of surgical denervation of one kidney on the ipsilateral efferent renal nerve activity (ERNA), in the absence of contralateral afferent renal nerve activity. Thus the ipsilateral renal denervation was performed 1 h later than the contralateral renal denervation. The experiments were done on 9 anesthetized cats. Arterial pressure, urine flow rate (UFR) of both kidneys and ERNA to the ipsilateral kidney were measured. All variables were monitored during a 3 min control period and for 13 min after either contralateral and ipsilateral renal denervations. ERNA significantly increased (+20 +/- 9%) and UFR concomitantly decreased (-11 +/- 10%) after the surgical denervation of the contralateral kidney which showed an increase (+91 +/- 19%) in UFR. The subsequent ipsilateral denervation caused a significant increase in UFR (+117 +/- 25%) and ERNA (79 +/- 23%) of the same kidney, while on the opposite side UFR did not change. During the two procedures, arterial pressure did not change. Our data demonstrate the existence of ipsilateral reno-renal reflexes that exert a tonic inhibitory effect on ipsilateral ERNA.

Renal afferents signaling diuretic activity in the cat.

Mechanoreceptors and chemoreceptors have been identified inside the kidney, but their functional role is still largely unclear. The aim of this study was to investigate whether changes in urine output could modify the discharge rate of renal afferent fibers. Experiments were performed in anesthetized cats in which afferent renal nerve activity (ARNA) was recorded by standard electrophysiological techniques from a centrally cut renal nerve. Arterial pressure, renal blood flow velocity, urine flow rate, and renal pelvic pressure were also measured. Three diuretic maneuvers were tested in the same cat: intravenous administration of physiological saline (8 to 13 mL/min for 2 minutes), furosemide (1 mg/kg), and atrial natriuretic peptide (ANP, 1 microgram/kg). The three maneuvers increased urine flow rate and pelvic pressure, respectively, 137.0 +/- 20.6% and 136.8 +/- 21.1% (saline), 148.6 +/- 31.7% and 139.6 +/- 43.5% (furosemide), and 75.9 +/- 7.9% and 62.1 +/- 21.2% (ANP) at the time of the maximum response. Arterial pressure slightly increased after saline, did not change after furosemide, and slightly decreased after ANP. Renal blood flow increased after saline and did not change after furosemide and ANP. The three maneuvers increased ARNA by 98.4 +/- 15.2% (saline), 270.7 +/- 100.8% (furosemide), and 59.6 +/- 23.4% (ANP). Changes in ARNA significantly correlate with changes in both pelvic pressure and urine flow rate. Our data demonstrate that increments in urine flow rate increase the firing rate of renal afferent fibers and suggest that (1) pelvic pressure is the major determinant of the neural response, and (2) this increased afferent discharge is due to activation of renal mechanoreceptors.

Angiotensin converting enzyme inhibition and renin release from the kidney.

Experiments were performed in anaesthetized cats, to determine whether renal nerves interfere with the negative feedback action of angiotensin II (Ang II) on renin release. The increase in renin release from the innervated kidney in response to captopril-induced inhibition of Ang II generation was compared with the response of the contralateral denervated kidney. Renin release was measured before (control), and 5, 15 and 30 min after the beginning of captopril infusion (1 mg/kg priming dose followed by 1 mg/kg per h for 30 min intravenously), and 60 min after the end of the infusion. During the captopril treatment renin release from both kidneys increased, but after 15 and 30 min the increase in renin release from the innervated kidneys was significantly larger than that observed in the denervated kidneys. After the captopril infusion was stopped, renin release from both kidneys returned towards control values. These results could not be explained on the basis of the changes in renal haemodynamics, excretory functions and efferent renal nerve activity observed during the captopril infusion. The data suggest that the renal nerves influence the changes in renin release caused by captopril by increasing the sensitivity of juxtaglomerular cells to the negative feedback action of Ang II.