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M J Kenney

Publications and source records attributed to M J Kenney.

34 records · Page 2Linked to original sources
PubMed1995

Sympathetic nerve responses to hyperthermia in the anesthetized rat.

The aim of the present study was to characterize the sympathetic nerve responses to hyperthermia in chloralose-anesthetized rats. Discharges were recorded from the renal, lumbar, and splanchnic sympathetic nerves. Mean arterial pressure, heart rate, and sympathetic nerve discharge (SND) were recorded continuously during progressive increases in core body temperature (Tc) from 38.0 to 41.0 degrees C. The following observations were made: 1) significant increases in renal, lumbar, and splanchnic SND were observed during hyperthermia; 2) autospectral analysis of renal and lumbar SND revealed that the frequency distribution of SND can be altered during progressive increases in Tc; and 3) increases in splanchnic SND to acute heating were similar in baroreceptor-innervated and -denervated rats. We conclude that 1) hyperthermia is a potent stimulus to the sympathetic nervous system and increases the activity in three sympathetic nerves that innervate different regional arterial beds, 2) acute heating influences the neural circuits involved in generating SND as evidenced by changes in the basic pattern of renal and lumbar SND, and 3) the increase in splanchnic SND during hyperthermia is not opposed by the arterial and cardiopulmonary baroreceptors.

Animals↗
PubMed1994

Frequency characteristics of sympathetic nerve discharge in anesthetized rats.

Frequency-domain analyses were used to characterize basal sympathetic nerve discharge (SND) and to determine the relationships between the activity recorded simultaneously from sympathetic nerves in chloralose-anesthetized, baroreceptor-innervated rats. Discharges were recorded from the splanchnic, renal, and lumbar nerves. The following observations were made. 1) Approximately 65-75% of total power in SND was contained below 9 Hz in either baroreceptor-innervated rats or baroreceptor-denervated rats. 2) Coherence values relating the activity of two nerves were significantly different from zero within this frequency band. 3) The interval between the discharges of two sympathetic nerves was either frequency dependent or constant within the coherent frequency band. 4) The frequency components of SND and the relationships between the activity in two sympathetic nerves could be altered during periods of acute stress. These results suggest that the system responsible for basal SND in rats is composed of either multiple sympathetic generators or multiple filters arranged in parallel, which are capable of producing different outputs. The dynamic nature of these circuits was revealed by the changes that occurred during periods of acute stress.

Acute Disease↗
PubMed1994

Sustained increases in aortic depressor nerve activity after acute elevation in arterial pressure.

OBJECTIVE: Despite the return of mean arterial pressure (MAP) to control levels, aortic depressor nerve activity remains elevated from control levels after sustained phenylephrine-induced increases in MAP in spontaneously hypertensive rats (SHR) (Kenney MJ, Morgan DA, Mark AL: Am J Physiol 1990, 258:H1476-H1481). This suggests that sustained increases in arterial pressure may produce prolonged pressure-induced changes in afferent baroreceptor nerve activity in SHR. However, because phenylephrine can exert an excitatory effect on the aortic arch baroreceptors, the increase in aortic depressor nerve activity might have resulted from a persistent direct effect of phenylephrine. The aim of the current study was to determine whether elevations in MAP induced by aortic occlusion produce increases in aortic depressor nerve activity which persist after the return of MAP to control levels. METHODS: MAP and aortic depressor nerve activity were recorded before, during and after sustained (15-30 min) periods of aortic occlusion in SHR with intact adrenal glands (n = 18) and in adrenalectomized SHR (n = 10). Control experiments were completed in which the same variables were recorded before, during and after sham aortic occlusion in intact (n = 8) and adrenalectomized (n = 8) SHR. RESULTS: Aortic occlusion increased MAP and aortic depressor nerve activity significantly from control levels. After aortic occlusion and the return of MAP to control levels, aortic depressor nerve activity remained significantly increased in 15 experiments, whereas in three experiments aortic depressor nerve activity was reduced. Aortic depressor nerve activity was increased significantly from control levels after aortic occlusion in adrenalectomized rats. Aortic depressor nerve activity remained unchanged from control levels after sham aortic occlusion in intact and adrenalectomized SHR. CONCLUSIONS: Sustained elevations in MAP induce increases in aortic depressor nerve activity in intact and adrenalectomized SHR, which persist after the return of MAP to control levels. These observations suggest that sustained increases in arterial pressure may produce prolonged pressure-induced changes in afferent baroreceptor nerve activity in SHR.

Adrenal Glands↗
PubMed1994

Influence of different preamplifier bandpass cutoff frequencies on the basic pattern of sympathetic nerve discharge.

Autospectral analysis reveals that most of the power in sympathetic nerve discharge (SND) is contained between 1 and 10 Hz in anesthetized animals. The synchronized discharge bursts of the fibers comprising sympathetic nerves are usually recorded after capacity-coupled preamplification with a bandpass of 1-1000 Hz. However, cardiac- and respiratory-related movement artifacts can adversely affect the signal when this wide bandpass (1-1000 Hz) is used. To eliminate the influence of movement artifacts on the basic pattern of SND, we have routed the output of a preamplifier (bandpass 30-1000 Hz) through a frequency analyzer which measures the frequency of spike discharges exceeding a threshold voltage. After the impulses are rectified and integrated a smooth envelope of the synchronized sympathetic nerve discharge bursts is produced. The following observations have been made: 1) The autospectra of SND constructed after either wide-band preamplification or 30-1000 Hz using the frequency analyzer are similar and 2) Narrow-band preamplification (30-1000 Hz) eliminates movement-related artifacts which adversely influence the sympathetic nerve signal. These results indicate that the basic pattern of SND can be faithfully recorded after narrow-band preamplification which eliminates potential movement-related artifacts.

Action Potentials↗
PubMed1993

Sciatic nerve stimulation induces hypotension but not renal or lumbar sympathoinhibition in hypertensive Dahl rats.

Sustained reductions in arterial pressure and sympathetic nerve activity occur after prolonged sciatic nerve stimulation in spontaneously hypertensive and pre-hypertensive Dahl salt-sensitive rats whereas these responses are not observed in renal hypertensive or Dahl resistant rats. These observations suggest that the development of post-stimulation hypotension and sympathoinhibition may be related to the genetic predisposition for hypertension rather than to the increased level of arterial pressure. However, it is not known whether the magnitude of the post-stimulation blood pressure and sympathetic nerve responses are influenced by the increased level of arterial pressure in addition to the genetic predisposition to hypertension. In the present study, we sought to determine if sustained sciatic nerve stimulation induces post-stimulation hypotension in hypertensive Dahl sensitive (DS) rats. For this purpose, mean arterial pressure (MAP), heart rate (HR), renal (RSNA) and lumbar (LSNA) sympathetic nerve activity were recorded during and after sciatic nerve stimulation in hypertensive DS rats (n = 17) fed an 8.0% NaCl diet for 7-8 weeks. Sciatic nerve stimulation increased HR (control, 443 +/- 10 b.p.m.; stimulation, 487 +/- 8 b.p.m.; p < 0.05) and tended to increase MAP, RSNA and LSNA. Two hours after stimulation, MAP was reduced (control 145 +/- 5 mmHg; recovery, 124 +/- 8 mmHg; p < 0.01) from control values. In contrast, RSNA and HR remained unchanged whereas LSNA was increased (69 +/- 20%; p < 0.05) from control values 120 min after stimulation. MAP, HR and RSNA were unchanged from control values during and for 2 h after sham stimulation in eight DS rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1993

Arterial baroreceptors and brain histamine contribute to bradycardia to peripheral hyperosmolality.

The purpose of this study was to determine whether the bradycardic response to peripheral hyperosmolality in conscious rats is dependent on afferent baroreceptor mechanisms and whether central histamine H2 receptors play a role in baroreflex-mediated changes in heart rate (HR). Mean arterial pressure (MAP) and HR were recorded continuously during a 30-min infusion of 2.5 M NaCl (10 microliters.100 g-1.min-1) hypertonic saline (HTS). HTS infusion significantly increased MAP (21 +/- 4 mmHg) and reduced HR (-62 +/- 10 beats/min) in rats with intact arterial baroreceptors. In sinoaortic-denervated rats, HR remained unchanged from control despite a significant increase in MAP. After intracerebroventricular (lateral ventricle) administration of cimetidine or ranitidine (H2-receptor antagonists) in intact rats, HTS infusion significantly increased MAP (19 +/- 2 and 17 +/- 2 mmHg, respectively) but the bradycardia was abolished (-12 +/- 10 and -10 +/- 10 beats/min, respectively). In contrast, central H2-receptor blockade did not alter reflex HR responses to the intravenous administration of phenylephrine and nitroprusside or to the central administration of histamine or angiotensin II. These results indicate that the bradycardic response to HTS infusion is mediated through the arterial baroreceptor reflex and involves in part a selective histaminergic pathway.

Angiotensin II↗
PubMed1993

Postexercise hypotension. Key features, mechanisms, and clinical significance.

Recent investigations have demonstrated that there is a sustained reduction in arterial blood pressure after a single bout of exercise, ie, postexercise hypotension (PEH). The purpose of this discussion is to integrate the available information on this topic and to review studies using sustained stimulation of somatic afferents in experimental rats as a model to study the role of somatic afferents in PEH. PEH occurs in response to several types of large-muscle dynamic exercise (ie, walking, running, leg cycling, and swimming) at submaximal intensities greater than 40% of peak aerobic capacity and exercise durations generally between 20 and 60 minutes. PEH is observed in both normotensive and hypertensive humans and in spontaneously hypertensive rats but is generally greater in magnitude in hypertensive subjects. The maximal exercise-induced reductions in systolic and diastolic arterial blood pressures have been on average 18 to 20 and 7 to 9 mm Hg, respectively, in hypertensive humans and 8 to 10 and 3 to 5 mm Hg, respectively, in normotensive humans. PEH has been reported to persist for 2 to 4 hours under laboratory conditions. Whether PEH is sustained for a prolonged period of time under free-living conditions remains controversial, although the results of one study indicate that PEH can persist for up to 13 hours. Possible mechanisms involved in mediating postexercise and poststimulation reductions in arterial blood pressure include decreased stroke volume and cardiac output; reductions in limb vascular resistance, total peripheral resistance, and muscle sympathetic nerve discharge; group III somatic afferent activation; altered baroreceptor reflex circulatory control; reduced vascular responsiveness to alpha-adrenergic receptor-mediated stimulation; and activation of endogenous opioid and serotonergic systems. It appears that the magnitude of PEH in hypertensive subjects is clinically significant; however, more investigation is required to determine if the duration is sufficient under real-life conditions to contribute to the reduction in blood pressure observed with chronic exercise conditioning.

Adult↗
PubMed1991

High power, low frequency components of cardiac, renal, splenic and vertebral sympathetic nerve activities are uniformly reduced by spinal cord transection.

Others have reported that spinal cord transection non-uniformly affects the activities of the cardiac, renal and splenic nerves. We were unable to confirm this finding while recording the wide band (1-1000 Hz) discharges of these sympathetic nerves in baroreceptor-denervated, chloralose-anesthetized cats. Most of the power in nerve discharges was below 6 Hz. There was high coherence between the low frequency discharges of different nerves, and power below 15 Hz was essentially eliminated by spinal transection. Evidence is presented that the disparities between this and past studies are, in part, due to the use of a 30-Hz high-pass filter in the earlier studies.

Animals↗
PubMed1991

Differential relationships among discharges of postganglionic sympathetic nerves.

The relationships among the simultaneously recorded discharges of as many as four postganglionic sympathetic nerves were studied with coherence and phase spectral analyses in baroreceptor-denervated cats. Discharges were recorded from the inferior cardiac (CN), vertebral (VN), and renal (RN) nerves. Most of the power in sympathetic nerve discharge was less than 6 Hz, and the discharges of any two nerves coherred over a frequency band generally between 0 and 15 Hz. Peak coherence occurred between 2 and 6 Hz in most cases. Our most important observations are as follows. 1) Coherence values were significantly higher in chloralose-anesthetized than in unanesthetized decerebrate cats. 2) Coherence values were higher for near ipsilateral nerves (e.g., CN and VN) than for widely separated ipsilateral nerves (e.g., CN and RN). 3) Coherence values for most pairs were higher when the nerves were located on the same side (ipsilateral nerves) rather than on opposite sides (contralateral nerves) of the body. 4) Coherence values were higher for some functionally complementary nerves (e.g., CN and RN) than for noncomplementary nerves (e.g., VN and RN). These results support the hypothesis that the central circuits responsible for the basal discharges of different postganglionic sympathetic nerves are selectively coupled.

Action Potentials↗
PubMed1991

Sympathetic nerve responses to sustained stimulation of somatic afferents in Dahl rats.

We tested the hypothesis that the hypotensive and sympathoinhibitory responses which occur after somatic afferent stimulation would be augmented in prehypertensive rats genetically predisposed to hypertension (Dahl salt-sensitive, DS) compared with rats resistant to the development of hypertension (Dahl salt-resistant, DR). For this purpose, we recorded mean arterial pressure (MAP), heart rate and renal sympathetic nerve activity (RSNA) during and following 30-min sciatic nerve stimulation in DS and DR rats fed a 0.4% NaCl diet. Baseline MAP did not differ significantly in the DS and DR rats. Somatic afferent stimulation in DS rats increased (P less than 0.05) MAP and heart rate and tended to increase RSNA whereas, in DR rats, stimulation increased (P less than 0.05) heart rate and tended to increase RSNA and MAP. Following somatic afferent stimulation, there were significant reductions (P less than 0.05) in both MAP (-20 +/- 6 mmHg) and RSNA (-36 +/- 8%) in DS rats. In contrast, DR rats did not exhibit significant poststimulation changes in MAP, and RSNA remained elevated from control following somatic afferent stimulation. These results suggest that the poststimulation inhibition of RSNA in DS rats may be related to the genetic predisposition of these rats to develop hypertension.

Afferent Pathways↗
PubMed1990

Prolonged renal sympathoinhibition following sustained elevation in arterial pressure.

We tested the hypothesis that sustained elevations in mean arterial pressure (MAP) would produce an abbreviated suppression of renal sympathetic nerve activity (RSNA) in spontaneously hypertensive (SH) compared with Wistar-Kyoto (WKY) normotensive rats. For this purpose, we recorded RSNA during and after a 30-min elevation in MAP. Elevations in MAP (35-40 mmHg) induced by phenylephrine resulted in a suppression of RSNA in SH and WKY rats that persisted after MAP had returned to control levels. The prolonged suppression of RSNA was eliminated following sinoaortic denervation, indicating that this response was dependent on afferent baroreceptor mechanisms. The simultaneous recording of RSNA and aortic depressor nerve (ADN) activity provided additional evidence that baroreceptor afferents contribute to this prolonged suppression of RSNA in SH rats. Despite the return of MAP to control levels following the sustained pressure elevation in SH rats, there was a paradoxical increase in ADN activity (39 +/- 14%) compared with control values. In contrast, both ADN activity and MAP returned to control levels in WKY rats following the sustained pressure elevation. The sustained increase of ADN activity in SH rats did not account for the entire magnitude of the prolonged recovery of RSNA. In summary, both SH and WKY rats exhibit prolonged suppression of RSNA, whereas ADN activity is paradoxically elevated in only SH rats following a sustained elevation in MAP.

Animals↗
PubMed1990

Relationships between activity of sympathetic nerve pairs: phase and coherence.

The coherence function and phase spectrum were used to study the relationships between the discharges of sets of two postganglionic or preganglionic sympathetic nerves in baroreceptor-denervated cats anesthetized with either 5,5-diallylbarbiturate-urethan or alpha-chloralose. Most of the power in sympathetic nerve discharge was contained between 2 and 6 Hz. The coherence values relating the activity of two nerves were significantly different from zero within this frequency band. The phase spectrum was either linear or complex (i.e., showed changes in slope) within the coherent frequency band. We observed three patterns of relationship. The first pattern was characterized by a constant interval between activity in different sympathetic nerves within the coherent frequency band. The second pattern was characterized by a frequency-dependent interval. The third pattern was characterized by uncoupling of the 2- to 6-Hz rhythms in the discharges of different nerves. Switching between these patterns was observed. We suggest that the three patterns reflect different functional states of the central system responsible for the 2- to 6-Hz rhythm. Two models of this system are entertained. The first model is one of a system of coupled oscillators while filtering circuits that receive common inputs are the elements of the second model.

Animals↗
PubMed1990

Forebrain rhythm generators influence sympathetic activity in anesthetized cats.

Autospectral and coherence analyses were used to study the frequency-domain relationships between frontal-parietal cortical activity [electroencephalogram (EEG)] and the discharges of the interior cardiac and renal sympathetic nerves of baroreceptor-denervated and vagotomized cats anesthetized with either alpha-chloralose or pentobarbital sodium. Delta slow-wave activity in the EEG was correlated to sympathetic nerve discharge (SND) as shown by sharp peaks between 0.5 and 4 Hz in the coherence function. The relationship was stronger in chloralose- than in pentobarbital-anesthetized cats. Coherence of the two signals could be attributed to descending influences of forebrain delta slow-wave generators on sympathetic circuits, since midbrain transection preferentially reduced the power in SND at frequencies that cohered to the EEG before transection. In contrast, the power in the EEG was not reduced by midbrain transection. The relationship between cortical delta slow-wave activity and SND was stronger during than between cortical spindlelike events that lasted 1-3 s and recurred once every 5-10 s. These events were similar to cortical spindles observed during the early stages of sleep and under light barbiturate anesthesia. These observations raise the possibility that the influences of forebrain delta slow-wave generators on SND are gated by thalamic mechanisms normally involved in the sleep-wake cycle.

Anesthesia↗
PubMed1988

Changes in jejunal myoelectrical activity during exercise in fed untrained dogs.

Seven female dogs (15-20 kg) were instrumented with seven bipolar electrodes sutured at 3-cm intervals to the serosal surface of the proximal jejunum and were exercised at different intensities and durations on a motor-driven treadmill. Slow-wave frequency increased (P less than 0.05) from preexercise control during prolonged (90 min) exercise and during recovery after short-term exercise (30 min) at 70% heart rate reserve (HRR). These changes were associated with an increase in core temperature. Spike-burst frequency (SBF) increased (P less than 0.05) with moderate exercise (50% HRR), but the magnitude was small. When exercise was extended beyond 30 min and during all recovery periods, SBF decreased significantly. Exercise produced migrating myoelectrical complexes in three experiments and less dramatic pattern changes characterized as "clustered contractions" (regular spike bursts preceded and followed by the absence of spike bursts) in at least nine other experiments. We conclude that exercise does alter jejunal myoelectrical activity, but myoelectrical patterns may be more important in explaining exercise-induced gastrointestinal symptoms than changes in spike-burst frequency or duration.

Animals↗