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Biomedical subjects

J Y Pan

Publications and source records attributed to J Y Pan.

51 records · Page 3Linked to original sources
PubMed1989

[Effects of intracisternal injection of naloxone on the depressor response to stimulation of renal afferent nerve in rabbits].

The purpose of this study was to observe the effects of opioid receptor and alpha-adrenergic receptors in the lower brain stem on the depressor response to electrical stimulation of renal afferent nerve, using intracisternal injection of blockers of these receptors. Experiments were conducted in sodium pentobarbital-anesthetized rabbits. The intracisternal injection (ict) of artificial cerebrospinal fluid (CSF) did not greatly affect the depressor response to stimulation of renal afferent nerve (RAS) and of aortic nerve (ANS). Ict of 550 nmol naloxone significantly inhibited the depressor response to RAS (P less than 0.05) but enhanced the depressor response to ANS (P less than 0.05). Ict of 335 nmol phentolamine significantly inhibited the depressor response to both RAS and ANS. Ict of naloxone reversed the phentolamine inhibition of the depressor response to ANS but did not affect the phentolamine inhibition of the depressor response to RAS. Ict of both naloxone and phentolamine did not affect the inhibitory interaction between the RAS-induced depressor and aortic baroreflex. Ict of phentolamine significantly decreased MAP, and ict of naloxone did not decrease MAP but reversed the decrease in MAP by ict of phentolamine. These data suggest that the activation of opioid receptors in the lower brain stem enhances the depressor response to RAS and attenuates the depressor response to ANS. Moreover, activation of alpha-adrenergic receptors in the lower brain stem facilitates the depressor response to RAS and ANS.

Animals↗
PubMed1985

Molecular cloning and sequencing of H-2Kk cDNA: comparison with other H-2 genes and evidence for alternative splicing.

A cDNA library was constructed from mouse L cells that were transfected with a human HLA-B7 gene fragment lacking the 5'-segment of exon 2 and all upstream sequences. A cDNA clone (pESP-C103) which is of mouse origin was detected by hybridization with the HLA-B7 gene. Comparison of the amino acid (aa) sequence predicted from the nucleotide sequence of the cDNA and the partial aa sequence of the H-2Kk antigen suggests that this cDNA (pESP-C103) codes for the H-2Kk antigen. This cDNA clone extends to the middle of the leader sequence. Comparison of the nucleotide and deduced aa sequences with those of other H-2 genes revealed an alternative splicing in exon 8 in the case of the H-2Kk gene.

Amino Acid Sequence↗
PubMed1985

Baroreflex control of sympathetic nerve activity after elevations of pressure in conscious rabbits.

The purpose of this study was to assess the effect of rapid baroreceptor resetting on the baroreflex control of renal sympathetic nerve activity in conscious rabbits. Renal sympathetic nerve activity was recorded and used as an index of the efferent limb of the baroreflex. Heart rate and arterial pressure were also recorded. Arterial pressure was raised with either phenylephrine or angiotensin II to a level that eliminated renal sympathetic nerve activity and was maintained at this level for periods of time ranging from 1 to 60 min. On returning pressure to control levels, renal sympathetic nerve activity remained suppressed for up to 90 min, with the duration of the suppression dependent on the magnitude and duration of the pressure stimulus. During this period of suppressed nerve activity, baroreflex curves were generated. The curves produced at this time were also suppressed as compared with control baroreflex curves. With time, the suppressed baroreflex curves returned to control. Further studies were performed to show that the suppression of renal sympathetic nerve activity was mediated via the prolonged increase in baroreceptor afferent activity during the pressure stimulus and was not due to a central effect of phenylephrine. This study indicates that although baroreceptor afferent activity may reset rapidly, there does not appear to be an augmentation of renal sympathetic nerve activity as would be expected.

Animals↗
PubMedDate not supplied

Inability of dorsal spinal rhizotomy to prevent renal wrap hypertension in rats.

Renal hypertension has been shown to be prevented and reversed by renal denervation. It has been postulated that the afferent nerves from the kidney are responsible for mediating the hypertensive stimulus that activates the sympathetic nervous system and increases arterial pressure. This study was designed to directly test the hypothesis that the afferent renal nerves are necessary for the development and maintenance of renal hypertension. In the first experiment, dorsal spinal rhizotomies or sham rhizotomies were performed in rats between T9 and L1, through which afferent renal nerves have been shown to traverse. After the one-kidney, one-wrap procedure, the increase in systolic arterial pressure and water intake was similar in the two groups of rats. To determine whether the removal of afferent renal nerves reversed the hypertensive process, animals with established renal hypertension were subjected to dorsal rhizotomy or the sham-rhizotomy procedure. Again, there was no significant effect on systolic arterial pressure and water intake. Although combined dorsal and ventral rhizotomy and subdiaphragmatic vagotomy did not affect the onset of hypertension, spinal transection at the level of C8 effectively prevented the rise in arterial pressure. Although efferent neural mechanisms contribute to the hypertensive process, these studies suggest that afferent renal nerves are not directly involved in the development and maintenance of one-kidney, one-wrap renal hypertension.

Afferent Pathways↗