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Biomedical subjects

H N Sapru

Publications and source records attributed to H N Sapru.

83 records · Page 5Linked to original sources
PubMed1976

Modification of aortic barorecptor resetting in the spontaneously hypertensive rat.

Aortic barorecptor function was studied in spontaneously hypertensive rats (SHR) of various ages and normotensive Wistar rats. The aortic arch was isolated and perfused, and the activity of the left aortic nerve was recorded. The threshold pressure to elicit barerecptor firing was 80-120 mmHg in normotensive Wistar rats. Resetting of barorecptors (threshold pressure 160-180 mmHg) was found in all untreated SHR of 35-70 wk of age. Resetting of barorecptors was prevented in SHR by starting treatment with antihypertensive agents at the age of 11 wk. Treatment of 32-wk old SHR with antihypertensive agents for 4-6 wk resulted in reversal of barorecptor resetting in 50% animals. The percentage of SHR showing complete reversal of resetting did not increase even when the duration of treatment was tripled. In 52- to 64-wk old SHR, treated with antihypertensive agents, reversal of baroceptor resetting was seen in only 30% animals. It was concluded that baroceptor resetting in SHR was secondary to hypertension. Hypertension, in turn, induced hypertrophy of the tunica media of the aorta. Histological studies showed a close correlation between aortic hypertrophy resetting. Aortic hypertrophy may, therefore, be one of the important factors involved in baroceptor resetting.

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Procedure for the decerebration of the rat.

A procedure for the decerebration of the rat was devised. The internal and external carotid arteries were ligated under halothane anesthesia. A transection was made at the mid-collicular level of the brain and the transected forebrain was removed. The posterior communicating arteries were occluded by suction and oxidized cellulose was packed around these vessels. The cut surface of the brain was covered with oxidized cellulose and the cranial cavity was filled with cotton balls. Head-up tilt, carotid occlusion and sodium cyanide responses indicated that the orthostatic, baro-, and chemo- reflexes were intact in these preparations. The stability of the preparation (for at least 8-10 hr) and the integrity of these reflexes indicate that the decerebrate rat may be a suitable alternative for studies involving brain stem regulatory mechanisms in this species when it is desirable to avoid general anesthetics.

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PubMedDate not supplied

Glutamate circuits in selected medullo-spinal areas regulating cardiovascular function.

1. The importance of the medullo-spinal neuronal pools in the regulation of cardiovascular function has been known for a long time. However, important groups of these neurons, interconnections between them and the neurotransmitters released at their projections have been identified with certainty only during the past two decades. 2. Some of the medullo-spinal neuronal pools mediating cardiovascular function include the nucleus tractus solitarius, caudal ventrolateral medullary depressor area, rostral ventrolateral medullary pressor area, nucleus ambiguus and intermediolateral cell column of the thoracolumbar spinal cord. Interactions between these selected neuronal groups and neurotransmitters in the pathways connecting them are discussed in the present short review.

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Blood pressure and splanchnic nerve activity are reduced by a vagally mediated opioid action.

An enkephalin analogue, D-Ala2-Met5-enkephalinamide (DAME), caused a fall in blood pressure (BP) following right atrial administration (RA) in urethane-anesthetized rats that were also atropinized, paralyzed, and artificially ventilated. This reduction in BP was not related to opioid-induced bradycardia. At a dose of 250 micrograms/kg RA the maximum percentage change was -36.0 +/- 3.9% occurring within 10-15 s subsequent to administration. The fall in BP was blocked by both pretreatment with naloxone HCl (75-100 micrograms/kg i.v.) and bilateral cervical vagotomy. Similar hypotensive responses (-37.3 +/- 2.3%) were obtained with phenyldiguanide (PDG) (40 micrograms/kg RA), a known stimulant of pulmonary J receptors (pulmonary C fibers). However, unlike DAME, the PDG response could not be blocked by naloxone. The fall in BP. obtained with DAME and PDG, paralleled a reduction in the spike frequency of the greater splanchnic nerve activity. This reflex fall in activity did not involve supramesencephalic structures because results were similar in both urethane-anesthetized and unanesthetized midcollicular decerebrate preparations. It was concluded that opioids can act peripherally, via pulmonary opiate receptors, to inhibit central vasomotor activity and reduce BP by eliciting a pulmonary chemoreflex.

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GABAergic mechanisms in the ventrolateral medulla alter vasopressor responses from the anterior hypothalamus.

The facilitatory and inhibitory roles of the ventrolateral medulla in modulating cardiovascular responses elicited from the anterior hypothalamus were studied in urethane-anesthetized rats. Control pressor responses (35-50 mm Hg) were consistently evoked by electrically stimulating the anterior hypothalamic medial preoptic area (AH/POA). The ventrolateral medulla is divided into two functionally distinct neuron pools, namely a rostral ventrolateral vasopressor area ( VLPA ) and a caudal ventrolateral vasodepressor area ( VLDA ). In each experiment neuron pools in the VLDA or VLPA were identified with bilateral microinjections of the neuroexcitatory amino acid L-glutamate, and changes in AH/POA responses were determined before and after alterations in ventrolateral neuronal activity. Inhibition or excitation of neuronal activity was accomplished by bilaterally stimulating or blocking gamma-aminobutyric acid (GABA) receptors, respectively, in the VLPA or VLDA . Inhibition of neuronal activity by microinjecting the GABA agonist muscimol into the VLPA decreased the AH/POA response by 64 +/- 10% and, in the VLDA , increased the AH/POA response by 57 +/- 4%. Blockade of GABA receptors by microinjecting the GABA antagonist bicuculline methiodide into the VLPA caused a 68 +/- 7% increase in the AH/POA response. Most surprising was a reversal of the AH/POA pressor response to a depressor response (150 + 2% decrease) following bicuculline microinjections in the VLDA . This finding suggests that GABA is released in the VLDA following AH/POA stimulation. It was concluded that neuron pools in the VLPA and VLDA determine the magnitude and direction of blood pressure responses elicited by electrical stimulation of the AH/POA. GABAergic mechanisms in the VLPA and the VLDA may modulate blood pressure changes relayed from the hypothalamus. A hypothetical pathway is proposed.

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Cardiovascular responses to medullary microinjections of opiate agonists in urethane-anesthetized rats.

Pressor (VLPA) and depressor (VLDA) areas of the ventrolateral medulla were identified by microinjections of L-glutamate in urethane-anesthetized rats. Cardiovascular effects of opiate agonists microinjected into the same sites were then studied. Agents used to stimulate mu, delta, sigma, kappa, and beta-endorphin (epsilon) receptors were morphiceptin, D-Ala2-D-Leu5-enkephalin, N-allyl-normetazocine, dynorphin, and beta-endorphin, respectively. Opiate receptor stimulation in VLPA decreased blood pressure (BP) and heart rate (HR), while in VLDA it increased BP and HR. Thus, it is the site of injection rather than the type of opiate receptor that determines cardiovascular responses. Naloxone, an opiate antagonist, reversed and prevented these responses. Abolition of cardiovascular responses by spinal transection at the C1 level indicated that the sympathetic nervous system mediated these responses. The following mechanism is proposed for these actions of opiates: Cell bodies in VLPA, but not in VLDA, project to the intermediolateral cell column of the spinal cord. Opiates inhibit VLPA and lower BP and HR by decreasing sympathetic outflow. Opiate-induced inhibition of VLDA, which has an inhibitory effect on VLPA, results in an increase in BP and HR.

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PubMedDate not supplied

Central resetting of baroreflex in the spontaneously hypertensive rat.

The role of central nervous system in the resetting of baroreflex was investigated in 5-month-old spontaneously hypertensive rats (SHR) of Okamoto strain. Age-matched Wistar-Kyoto (WKY) rats were used as normotensive controls. The aortic nerves, which in the rat, contain few or no chemoreceptor fibers, were stimulated electrically using a wide range of stimulus frequencies. The depressor responses (expressed as percent decrease in blood pressure as compared to its blood pressure value prior to aortic nerve stimulation) produced by these stimulations were significantly smaller in SHR than those in WKY. In another series of experiments, changes in the efferent limb of the baroreflex arc (i.e., greater splanchnic nerve activity) in response to stimulation of the baroreceptor afferents in the aortic nerve were recorded. Inhibition of the greater splanchnic nerve activity due to aortic nerve stimulation was found to be significantly smaller in SHR than in the WKY. Control sympathetic nerve activity was greater in SHR than in WKY. These results suggest that the central bulbospinal nervous system may be another site for resetting of baroreflex in hypertension.

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