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Biomedical subjects

B Brooks

Publications and source records attributed to B Brooks.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

Actions of galanin fragments on rat, guinea-pig, and canine intestinal motility.

The 1-20 fragment of synthetic porcine galanin, prepared by tryptic digestion of the intact molecule, was equipotent to synthetic porcine galanin 1-29 in the smooth muscle actions of exciting the rat jejunal longitudinal muscle in vitro and inhibiting circular muscle contractions of the canine small intestine in vitro and in vivo, but was less potent in inhibiting nerve-stimulated contractions of the guinea-pig taenia coli. Fragment 21-29 was effective at high doses only in the canine ileum. Activity of galanin 1-11 was greatly reduced in the dog in vivo. These results may reflect species or cell type differences.

Animals↗
PubMedDate not supplied

In vitro effects of recombinant human megakaryocyte growth and development factor on primary human tumour colony growth.

A study was made of the in vitro effects of recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) on breast, prostate, cervix and colon cancers. Tumour growth was assessed using a soft agar clonogenic assay. Stimulation of megakaryocyte numbers was seen in liquid culture following 10 ng/ml PEG-rHuMGDF. The same concentration led to no significant difference in colony-forming efficiencies for 22 of 25 tumour samples. A significant reduction in colony-forming efficiencies was seen for the remaining 3 specimens. These results suggest that PEG-rHuMGDF will not stimulate tumour growth in vivo.

Breast Neoplasms↗
PubMedDate not supplied

Renomedullary deficiency in partial nephrectomy-salt hypertension.

Partial nephrectomy-salt hypertension (PN-SH) of the rat is associated with Na volume loading. As the hypertensive state evolves, the renomedullary interstitial cells (RIC) of the renal nubbin undergo major changes, decreasing significantly in number while the remaining ones exhibit degenerative changes. The antihypertensive action of the RIC in the renal nubbin, as measured by transplants of fragmented papillae into hypertensive recipients, virtually disappears as the hypertension develops. The changes in the RIC occur whether vascular disease of the kidney is or is not overtly present. It is suggested that deficiency of the antihypertensive action of the RIC allows the prohypertensive effects of Na volume loading to operate without proper control. Thus, the sustained hypertensive state of this model does not appear to be due solely to volume expansion. Rather, it appears due to a combination of the effects of Na and volume and a renomedullary deficiency of hormonal type. The specific cause(s) of the changes in the RIC was not determined. It seems evident that it is related to the high salt intake since the partial nephrectomy procedure without the added salt load did not alter the appearance of the RIC.

Animals↗
PubMedDate not supplied

Alkyl ether analogs of phosphatidylcholine are orally active in hypertensive rabbits.

1-0-alkyl ethers of phosphatidylcholine having an acetoyl in the second position were derived from fresh renal tissue. The main ether so derived had a 16:0 chain. The C16:0 alkyl ether was synthesized de novo. The renally derived and the synthetic ether exerted a similar and powerful antihypertensive action in hypertensive rabbits when given orally in divided doses. This action was prolonged, requiring more than 60 hours after the last input of the compound for recovery of the arterial pressure. As these ethers exerted their antihypertensive action, there was no evidence of adverse effects. Noteworthy was the failure of these depressor compounds to cause renin release. Diuresis-kaliuresis did not occur. A suggestion of sodium retention was noted.

Administration, Oral↗
PubMedDate not supplied

Degranulation of renomedullary interstitial cells during reversal of hypertension.

It was demonstrated earlier that the renal venous effluent of one-kidney, one clip hypertensive rats contained a vasodepressor lipid resembling the antihypertensive neutral renomedullary lipid (ANRL), following unclipping and as the arterial pressure (MAP) was lowered. Consequently, the sham-unclipped (clip-intact) and the unclipped kidney (CK and UCK) were studied by electronmicroscopy and morphometrically (Weibel's techniques). Renomedullary interstitial cells (RIC) of the CK had abundant granules. The collecting duct (CD) had tall lining cells containing pale granules and displayed intercellular channels. Following unclipping, the RIC degranulated and the CD cells became flattened, lost their pale granules, and the intercellular channels disappeared as the MAP decreased. These changes were evident by EM appearance and volume density measurements. The renopapillary changes occurred as the kidney secreted the ANRL-like substance into the blood.

Animals↗
PubMedDate not supplied

Cardiovascular effects of antihypertensive polar and neutral renomedullary lipids.

Two antihypertensive lipids can be extracted from fresh renal medulla. One is polar (the antihypertensive polar renomedullary lipid, or APRL) and the other is nonpolar (the antihypertensive neutral renomedullary lipid, or ANRL). APRL and ANRL differ in their biologic activities: APRL in bolus intravenous injections causes a very rapid decline in the arterial pressure (AP) while ANRL, after a lag of 2 minutes, causes a slower decline in AP. APRL increases heart rate and sympathetic activity. ANRL decreases heart rate and sympathetic activity. ANRL appears to convert to APRL, under certain in vitro circumstances, suggesting that the structure of the two molecules is related. ANRL and APRL appear in the renal venous effluent after unclipping; biologically, ANRL seems dominant. The renal venous effluent of the unclipped isolated kidney lowers the HR and sympathetic activity of the normal rat. Unclipping degranulates the renomedullary interstitial cells (RIC). The antihypertensive effect of unclipping appears due to the secretion of ANRL and APRL by the kidney. It is concluded that ANRL seems to be the antihypertensive hormone of the RIC.

Animals↗
PubMedDate not supplied

Antihypertensive polar and neutral renopapillary lipids. Which is a hormone?

Two antihypertensive lipids can be derived from the renal papilla, the antihypertensive polar (APRL) and the antihypertensive neutral (ANRL) renomedullary lipid. The renal venous effluent of the unclipped kidney contains both ANRL and APRL. This effluent lowers the arterial pressure (AP) of the normal rat when infused i.v. As it lowers the AP the heart rate (HR) and sympathetic nerve activity (SNA) are depressed. ANRL infused i.v. also lowers HR and SNA as it depresses the AP. Conversely, APRL elevates HR and SNA as it lowers the AP. Thus, of the two lipids in the renal venous effluent after unclipping, ANRL appears to be dominant. APRL, however, in the renal venous effluent could potentiate the action of ANRL. The net effect of these observations is to support the view that ANRL is an antihypertensive hormone liberated by the kidney after unclipping. The renomedullary interstitial cells (RIC) degranulate after unclipping. ANRL can be derived from these cells. Thus, the RIC, cells known to exert an endocrine-type antihypertensive function, may well be the source of ANRL in the renal venous effluent after unclipping. The hormonal action of ANRL appears as a major cause of the lowering of the AP after unclipping. It is not known what factors modulate the RIC endocrine system. There is a suggestion that angiotensin may be one of these factors based on the ineffectiveness of these cells toward retarding hypertension when the circulating plasma angiotensin level is high, and their effectiveness when the circulating plasma angiotensin level is low.

Angiotensins↗