Cardiovascular and neurohormonal effects of intravenous adrenomedullin in conscious rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. R1289-R1293 ◽  
Author(s):  
M. Fukuhara ◽  
T. Tsuchihashi ◽  
I. Abe ◽  
M. Fujishima
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Conscious Rabbits ◽  
Renal Sympathetic

Adrenomedullin is a vasodilative peptide and shows slight homology with calcitonin gene-related peptide. In the present study, we investigated the effects of adrenomedullin on cardiovascular and neurohormonal responses in 13 conscious rabbits. The animals were chronically instrumented with bipolar electrodes on the left renal sympathetic nerve. Intravenous administration of human adrenomedullin (10, 100, 1,000, and 3,000 pmol/kg, n = 6) caused a dose-dependent reduction in mean arterial pressure (0 +/- 2, -1 +/- 2, -19 +/- 2, and -29 +/- 4 mmHg, respectively) concomitant with increases in heart rate, renal sympathetic nerve activity, plasma renin activity, and plasma norepinephrine. The significant reduction in mean arterial pressure induced by 1,000 pmol/kg of adrenomedullin occurred within 1 min after injection and lasted for 15 min (n = 7). In contrast, the significant increases in heart rate and renal sympathetic nerve activity lasted for more than 50 min. When mean arterial pressure was decreased by 15 mmHg by adrenomedullin, the increases in heart rate and renal sympathetic nerve activity were 53 +/- 8 beats/min and 78 +/- 13%, respectively, which were significantly smaller than those induced by intravenous injection of sodium nitroprusside (102 +/- 14 beats/min and 155 +/- 34%, respectively). These results suggest that intravenous adrenomedullin exerts a hypotensive action that is associated with the attenuated reflex-mediated sympathetic activation.

scholarly journals Cardiopulmonary baroreflex function in nephrotic rats.

1995 ◽  
Vol 5 (12) ◽  
pp. 2082-2086
Author(s):  
J C Neahring ◽  
S Y Jones ◽  
G F DiBona
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Cardiopulmonary Baroreflex ◽  
Renal Sympathetic

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.

scholarly journals Central effects of leptin on cardiovascular and neurohormonal responses in conscious rabbits

2000 ◽  
Vol 278 (5) ◽  
pp. R1314-R1320 ◽  
Author(s):  
Kiyoshi Matsumura ◽  
Isao Abe ◽  
Takuya Tsuchihashi ◽  
Masatoshi Fujishima
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Intracerebroventricular Injection ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Glucose Levels ◽  
Renal Sympathetic Nerve ◽  
Conscious Rabbits ◽  
Renal Sympathetic

We determined the cardiovascular and neurohormonal responses to intracerebroventricular injection of leptin in conscious rabbits. Intracerebroventricular injection of leptin elicited dose-related increases in mean arterial pressure and renal sympathetic nerve activity while producing no consistent, significant increases in heart rate. Peak values of mean arterial pressure and renal sympathetic nerve activity induced by intracerebroventricular injection of 50 μg of leptin (+17.3 ± 1.2 mmHg and +47.9 ± 12.0%) were obtained at 10 and 20 min after injection, respectively. Plasma catecholamine concentrations significantly increased at 60 min after intracerebroventricular injection of leptin (control vs. 60 min; epinephrine: 33 ± 12 vs. 97 ± 27 pg/ml, P < 0.05; norepinephrine: 298 ± 39 vs. 503 ± 86 pg/ml, P < 0.05). Intracerebroventricular injection of leptin also caused significant increases in plasma vasopressin and glucose levels. However, pretreatment with intravenous injection of pentolinium (5 mg/kg), a ganglion blocking agent, abolished these cardiovascular and neurohormonal responses. On the other hand, intravenous injection of the same dose of leptin (50 μg) as used in the intracerebroventricular experiment failed to cause any cardiovascular and renal sympathetic nerve responses. These results suggest that intracerebroventricular leptin acts in the central nervous system and activates sympathoadrenal outflow, resulting in increases in arterial pressure and plasma glucose levels in conscious rabbits.

Hemodynamic and sympathetic effects of spinal administration of neuropeptide Y in rats

1990 ◽  
Vol 259 (6) ◽  
pp. H1674-H1680 ◽  
Author(s):  
X. L. Chen ◽  
M. M. Knuepfer ◽  
T. C. Westfall
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Intrathecal Administration ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Intrathecal administration of 4 nmol/kg neuropeptide Y in Dial-urethane-anesthetized rats elicited decreases in arterial pressure, renal sympathetic nerve activity, and a slight decrease in heart rate. The depressor response was associated with a sustained hindquarters and mesenteric vasodilation resulting in a decrease in total peripheral resistance. Intrathecal NPY also resulted in a decrease in renal sympathetic nerve activity. There was a positive correlation between the percent changes in arterial pressure and renal sympathetic nerve activity. With the use of renal nerve activity and heart rate as indexes, NPY resulted in a decrease in baroreflex sensitivity. The depressor effect of intrathecal NPY did not appear to be due to spinal vasoconstriction and ischemia, since spinal microvascular resistance was decreased slightly. We conclude that the intrathecal administration of NPY produces an inhibition of sympathetic nerve activity, resulting in a decrease in total peripheral resistance and arterial pressure.

Renal nerve activity and renal function during environmental stress in DOCA-NaCl rats

1986 ◽  
Vol 251 (2) ◽  
pp. R289-R294 ◽  
Author(s):  
J. P. Koepke ◽  
S. Jones ◽  
G. F. DiBona
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Renal Denervation ◽  
Sympathetic Nerve Activity ◽  
Hypertensive Rats ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The effects of a stressful environmental stimulus (air stress) on mean arterial pressure, heart rate, renal sympathetic nerve activity, and renal function were studied in conscious deoxycorticosterone acetate-sodium chloride (DOCA-NaCl) hypertensive rats, sham DOCA-NaCl normotensive rats, and DOCA-NaCl rats with renal denervation. In conscious DOCA-NaCl hypertensive rats, air stress decreased urine flow rate [36% from 17.9 +/- 3.0 microliter X min-1 X 100 g body wt-1 (BW)], urinary sodium excretion (39% from 3.1 +/- 0.5 microeq X min-1 X 100 g BW-1), fractional water excretion (24% from 4.72 +/- 1.00%), and fractional sodium excretion (28% from 5.72 +/- 1.08%) and increased renal sympathetic nerve activity (94% from 8.3 +/- 0.6 integrator resets/min), but no changes occurred in glomerular filtration rate (-15% from 0.40 +/- 0.06 ml X min-1 X 100 g BW-1) or effective renal plasma flow (-7% from 2.50 +/- 0.53 ml X min-1 X 100 g BW-1). Air stress had no effect on these measures in conscious sham DOCA-NaCl normotensive rats or DOCA-NaCl rats with renal denervation. Mean arterial pressure and heart rate were unaffected by air stress in these three groups. Renal denervation lowered base-line mean arterial pressure in DOCA-NaCl rats. Thus DOCA-NaCl hypertensive rats respond to environmental stress with increased renal sympathetic nerve activity and, consequently, antidiuresis and antinatriuresis.

scholarly journals Hemodynamic defense response to thyrotropin-releasing hormone injected into medial preoptic nucleus in rats

1991 ◽  
Vol 261 (2) ◽  
pp. R305-R312 ◽  
Author(s):  
A. L. Siren ◽  
S. Vonhof ◽  
G. Feuerstein
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Defense Response ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

The role of thyrotropin-releasing hormone (TRH) and glutamate in central cardiovascular control was studied by microinjections (50 nl) of these agents into the medial or median preoptic nuclei of conscious rats (n = 49) with continuous recording of mean arterial pressure, heart rate, blood flow, and vascular resistance in hindquarter, renal, and mesenteric blood vessels. In addition, the effect of TRH on renal sympathetic nerve activity was studied in anesthetized rats. TRH (2.4-240 pmol) elicited the typical hemodynamic pattern of the "defense response" consisting of increased blood pressure, tachycardia, hindquarter vasodilation, and constriction of renal and mesenteric blood vessels. Maximum changes in cardiovascular variables after the 24-pmol dose were +12 +/- 2 mmHg (mean arterial pressure), +73 +/- 15 beats/min (heart rate), -21 +/- 6% (hindquarter resistance), +15 +/- 6% (renal resistance), and +31 +/- 6% (mesenteric resistance), P less than 0.05 compared with saline. In anesthetized rats, TRH at the 2.4-pmol dose increased renal sympathetic nerve activity (greater than 200%, n = 5, P less than 0.05 compared with control) with no effect on blood pressure or renal flow. Glutamate (10 or 100 nmol) produced a similar pattern of hemodynamic changes as TRH. Peak effects after the 100-nmol dose of glutamate were +16 +/- 2 mmHg (mean arterial pressure), +57 +/- 11 beats/min (heart rate), -31 +/- 3% (hindquarter resistance), +29 +/- 9% (renal resistance), and +87 +/- 22% (mesenteric resistance), P less than 0.05 compared with saline. The glutamate N-methyl-D-aspartate (NMDA) receptor blocker MK-801 (300 micrograms/kg iv) attenuated the pressor-tachycardic responses to TRH and the pressor-mesenteric constrictor responses to glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertonic sodium resuscitation after hemorrhage improves hemodynamic function by stimulating cardiac, but not renal, sympathetic nerve activity

2011 ◽  
Vol 300 (2) ◽  
pp. H685-H692 ◽  
Author(s):  
Robert Frithiof ◽  
Rohit Ramchandra ◽  
Sally G. Hood ◽  
Clive N. May
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Hypertonic Saline ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

Small volume hypertonic saline resuscitation can be beneficial for treating hemorrhagic shock, but the mechanism remains poorly defined. We investigated the effects of hemorrhagic resuscitation with hypertonic saline on cardiac (CSNA) and renal sympathetic nerve activity (RSNA) and the resulting cardiovascular consequences. Studies were performed on conscious sheep instrumented with cardiac ( n = 7) and renal ( n = 6) sympathetic nerve recording electrodes and a pulmonary artery flow probe. Hemorrhage (20 ml/kg over 20 min) caused hypotension and tachycardia followed by bradycardia, reduced cardiac output, and abolition of CSNA and RSNA. Resuscitation with intravenous hypertonic saline (1.2 mol/l at 2 ml/kg) caused rapid, dramatic increases in mean arterial pressure, heart rate, and CSNA, but had no effect on RSNA. In contrast, isotonic saline resuscitation (12 ml/kg) had a much delayed and smaller effect on CSNA, less effect on mean arterial pressure, no effect on heart rate, but stimulated RSNA, although the plasma volume expansion was similar. Intracarotid infusion of hypertonic saline (1 ml/min bilaterally, n = 5) caused similar changes to intravenous administration, indicating a cerebral component to the effects of hypertonic saline. In further experiments, contractility (maximum change in pressure over time), heart rate, and cardiac output increased significantly more with intravenous hypertonic saline (2 ml/kg) than with Gelofusine (6 ml/kg) after hemorrhage; the effects of hypertonic saline were attenuated by the β-receptor antagonist propranolol ( n = 6). These results demonstrate a novel neural mechanism for the effects of hypertonic saline resuscitation, comprising cerebral stimulation of CSNA by sodium chloride to improve cardiac output by increasing cardiac contractility and rate and inhibition of RSNA.

Increase in sympathetic outflow by paraventricular nucleus stimulation in awake rats

1989 ◽  
Vol 256 (6) ◽  
pp. R1325-R1330 ◽  
Author(s):  
H. Kannan ◽  
Y. Hayashida ◽  
H. Yamashita
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

Our previous studies demonstrated that stimulation of the hypothalamic paraventricular nucleus (PVN) in anesthetized rats evoked a depressor response accompanied with a decrease in sympathetic outflow (H. Kannan, A. Niijima, and H. Yamashita, J. Auton. Nerv. Syst. 19: 83-86, 1987; H. Yamashita, H. Kannan, M. Kasai, and T. Osaka, J. Auton. Nerv. Syst. 19: 229-234, 1987). Because anesthesia may alter cardiovascular responses, we examined in conscious rats the effects of PVN stimulation on arterial pressure, heart rate, and renal sympathetic nerve activity. Electrical stimulation through chronically implanted electrodes evoked increases in arterial pressure and renal sympathetic nerve activity with a slight decrease in heart rate. The magnitude of responses was dependent on the frequency and the intensity of the stimulus. Latency of the excitatory response of the renal sympathetic nerve activity was approximately 70 ms. Microinjection of L-glutamate (0.5 M, 200 nl) into the PVN area also elicited increases in blood pressure and renal sympathetic nerve activity. These results suggest that activation of PVN neurons in conscious rats produces pressor responses due to an increase in the sympathetic outflow. These findings contrast with those obtained previously in anesthetized rats.

Renal sympathetic nerve and hemodynamic responses to captopril in conscious dogs: role of prostaglandins

1991 ◽  
Vol 260 (1) ◽  
pp. H260-H266
Author(s):  
I. H. Zucker ◽  
J. S. Chen ◽  
W. Wang
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Enzyme Inhibitor ◽  
Cyclooxygenase Inhibitor ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic

The angiotensin converting enzyme inhibitor captopril has been shown to cause resetting of the arterial baroreflex to a lower pressure without a change in gain. The present study was conducted to determine whether captopril altered the relationship between arterial pressure, heart rate, and renal sympathetic nerve activity in conscious quietly resting dogs. Fourteen instrumented dogs were given 2 mg/kg iv of captopril; 10 min later postcaptopril measurements were made. Six of the fourteen dogs were pretreated with cyclooxygenase inhibitor (indomethacin or meclofenamate) before administration of captopril. Renal nerve activity and hemodynamics were measured in a final group of eight dogs in which arterial pressure was lowered with a graded infusion of sodium nitroprusside. Captopril caused a small but significant decrease in arterial pressure. This decrease in arterial pressure was accompanied by a significant increase in heart rate; however, renal sympathetic nerve activity was significantly reduced. In contrast, dogs receiving nitroprusside exhibited an increase in both heart rate and renal sympathetic nerve activity in response to similar decreases in arterial pressure. Dogs that received cyclooxygenase inhibitor showed reduced arterial pressure in response to captopril, increased heart rate, and increased renal sympathetic nerve activity. This study is the first to report a decrease in sympathetic nerve activity in response to captopril in an awake chronically instrumented animals. These data suggest that captopril's ability to augment prostaglandin synthesis is responsible for the observed sympathoinhibition.

Transfer function analysis between arterial pressure and renal sympathetic nerve activity at cardiac pacing frequencies in the rat

2007 ◽  
Vol 102 (3) ◽  
pp. 1034-1040 ◽  
Author(s):  
Valérie Oréa ◽  
Roy Kanbar ◽  
Bruno Chapuis ◽  
Christian Barrès ◽  
Claude Julien
Keyword(s):  
Transfer Function ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiac Pacing ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Baseline Conditions ◽  
Renal Sympathetic

This study examined the possible influence of changes in heart rate (HR) on the gain of the transfer function relating renal sympathetic nerve activity (RSNA) to arterial pressure (AP) at HR frequency in rats. In seven urethane-anesthetized rats, AP and RSNA were recorded under baseline conditions (spontaneous HR = 338 ± 6 beats/min, i.e., 5.6 ± 0.1 Hz) and during 70-s periods of cardiac pacing at 6–9 Hz applied in random order. Cardiac pacing slightly increased mean AP (0.8 ± 0.2 mmHg/Hz) and decreased pulse pressure (−3.6 ± 0.3 mmHg/Hz) while leaving the mean level of RSNA essentially unaltered ( P = 0.680, repeated-measures ANOVA). The gain of the transfer function from AP to RSNA measured at HR frequency was always associated with a strong, significant coherence and was stable between 6 and 9 Hz ( P = 0.185). The transfer function gain measured under baseline conditions [2.44 ± 0.28 normalized units (NU)/mmHg] did not differ from that measured during cardiac pacing (2.46 ± 0.27 NU/mmHg). On the contrary, phase decreased linearly as a function of HR, which indicated the presence of a fixed time delay (97 ± 6 ms) between AP and RSNA. In conclusion, the dynamic properties of arterial baroreflex pathways do not affect the gain of the transfer function between AP and RSNA measured at HR frequency in the upper part of the physiological range of HR variations in the rat.

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