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Biomedical subjects

G Göthberg

Publications and source records attributed to G Göthberg.

63 records · Page 4Linked to original sources
PubMed1979

Apparent and true vascular resistances to flow in SHR and NCR kidneys as related to the pre/postglomerular resistance ratio.

In maximally vasodilated SHR and NCR kidneys, perfused with filtrable and non-filtrable perfusates, analyses have been performed concerning the extent of average renal tissue pressure (Pt) elevation which occurs upon glomerular filtration and causes passive autoregulation of flow. The results illustrate the great importance of distinguishing between 'apparent' (PA--PV/flow) and 'true' (PA--Pt/flow) renal resistance to flow. This is particularly so when the compared SHR and NCR renal vascular beds differ not only in true total renal resistance but also concerning the structurally determined ratio between the pre- and post-glomerular resistances. The combined results show that this ratio is considerably elevated in adults SHT kidneys because of structural vascular changes, which is perhaps the most efficient way of resetting the 'long term barostat function' of the kidneys in hypertension. It is also illustrated how the altered pre-/post-glomerular ratio in SHR in combination with Pt rises can so markedly distort the results of apparently precise in vitro comparisons of SHR and NCR renal vascular beds as to give entirely misleading results, with underestimations of the structurally based vascular hyperreactivity of the preglomerular section in SHR.

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PubMed1976

Hemodynamic consequences of resistance vessel rarification and of changes in smooth muscle sensitivity.

Alterations in resistance vessel design in form of an increased wall/lumen ratio appears to markedly influence the resistance control in primary hypertension (Folkow et al. 1973). The raised resistance has also been suggested to be a consequence of a rarification of resistence vessels or/and to an increased vascular smooth muscle sensitivity. Thus two series paired experiments were performed on matched normotensive rats, utilizing the responses of their hindquarter vascular beds during constant flow perfusion. In the first series, the precapillary resistance vessels section was first "rarified" by graded microplugging, thereby raising resistance at maximal dilatation about 50 per cent. Then the vascular responses to noradrenaline were studied to characterize the dose-response or "resistance curves". In the second series the vascular smooth muscle sensitivity to noradrenaline of one of the hindquarters was changed by infusion of phentolamine. The resistance responses were then recorded and the ensuing "resistance curves" compared. --These changes of resistance vascular architecture and vascular smooth muscle sensitivity, respectively, led to mutually different characters of the "resistance curves". Both of these differ, however, in virtually all important respects from those curves characterizing vascular beds of spontaneously or renal hypertensive rats.

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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.

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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↗
PubMedDate not supplied

Consequences of structural renovascular changes for renal barostat function.

During maximal vasodilatation the renal vascular beds of normotensive control rats (NCR), uninephrectomized NCR (U-NCR), spontaneously hypertensive rats (SHR), and two-kidney, one clip renal hypertensive rats (RHR) have been compared concerning glomerular filtration capacity, total renovascular resistance, and the relationship between perfusion pressure and glomerular filtration rate (GFR). The GFR reflects the important ratio between the preglomerular and postglomerular resistances that is a major determinant of GFR, and during maximal vasodilatation it shows whether, and how, this ratio is altered by differentiated renovascular structural adaptation. In SHR hypertension this ratio soon becomes increased to match the pressure rise as a result of structural changes, which implies a most efficient upward resetting of the renal barostat function. Later the postglomerular resistance is also raised in SHR as a result of structural changes. This adaptation presumably occurs to offset the gradual deterioration in glomerular filtration capacity. In the clipped, "low-pressure" RHR kidney, only the preglomerular resistance is reduced, a local adaptation tending to offset the effect of the artificial inflow hindrance on GFR as a result of structural changes. In the "pressure-exposed" RHR kidney the preglomerular and postglomerular resistances are both equally increased, again as a result of structural changes. In this situation, therefore, resetting of the renal barostat function occurs less efficiently than in SHR. This may explain the observation that arterial pressure readily normalizes in RHR on declipping. The hypertrophic U-NCR kidney shows a proportional and uniform outgrowth of the renovascular bed, thus without altering the pre-postglomerular resistance ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

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