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Biomedical subjects

G Göthberg

Publications and source records attributed to G Göthberg.

At least 55 records · Page 3Linked to original sources
PubMed1988

Activation of the humoral antihypertensive system of the kidney increases diuresis.

Isolated kidneys taken from normotensive Wistar-Kyoto rats were cross-perfused extracorporeally by normotensive strain-matched donor rats. The extracorporeal perfusion circuit was arranged so that the perfusion pressure to the normotensive recipient kidney could be varied from 90 to 200 mm Hg without any change in total flow through this circuit. This setup avoided hemodynamic or mechanical interferences with reflexogenic circulatory control in the normotensive donor rat when the recipient kidney was manipulated. Diuresis and natriuresis were measured in the normotensive donor rat and the normotensive recipient kidney. A few minutes after normotensive recipient kidney perfusion pressure had been raised, mean arterial pressure (MAP) and heart rate started to decline rapidly in the normotensive donor rat, and circulatory collapse ensued within 15 to 100 minutes. During the control period at 90 mm Hg normotensive recipient kidney perfusion pressure, urinary flow, MAP and heart rate were stable in the normotensive donor rat and the normotensive recipient kidney. When perfusion pressure was raised to 200 mm Hg in the recipient kidney, the urinary flow in the donor rat increased 62% on average in the first 10 minutes over values recorded before the pressure rise (p less than 0.05) while MAP simultaneously fell by 16% and HR remained unchanged. During the subsequent period, the urinary flow of the donor rat declined together with MAP and heart rate. In the extracorporeally high-pressure perfused recipient kidneys, an eightfold to ninefold increase in diuresis and natriuresis occurred during the first 45 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The humorally mediated antihypertensive system of the rat kidney: a physiological depressor mechanism?

The humoral renomedullary antihypertensive system, described by Muirhead [1], is known to be strongly activated upon unclipping renal hypertensive rats. The present study was designed to determine whether this system is tonically active in normotensive rat kidneys at normotensive pressure levels. Anaesthetized normotensive donor rats (NDR) were used to perfuse an isolated age-matched normotensive recipient (NRR) kidney, via an extracorporal circuit, set at different perfusion pressures, while the NDR mean arterial pressure and heart rate were measured continuously. The results showed non-significant alterations in the NDR heart rate and mean arterial pressure at 80 mmHg NRR kidney perfusion pressure, while at 100 and 150 mmHg there were significant, dose-dependent and gradual reductions in both the heart rate and mean arterial pressure in NDR. We conclude that the renal humoral antihypertensive system is active in normotensive kidneys already in the normotensive pressure range, but becomes further engaged in a dose-dependent way when renal perfusion pressure is raised.

Animals↗
PubMed1986

Sympathetic inhibition after surgical reversal of renovascular hypertension in rats. Role of vagal nerves.

The present study was undertaken to study the changes in efferent renal sympathetic nerve activity (RSNA) and heart rate (HR) during the acute fall in blood pressure after surgical reversal of two-kidney, one-clip renovascular hypertension in rats, and to explore if cardiopulmonary vagal afferents can influence sympathetic outflow in this situation. In 14 rats with a MAP of 199 +/- 6 mmHg the renal artery clip was surgically removed and after 90 min MAP had decreased to 109 +/- 7 mmHg. The HR had then decreased by 26 +/- 15 beats min-1 (P less than 0.05) and RSNA did not increase as expected, but was somewhat reduced (84 +/- 8% of control). In contrast, lowering pressure with nitroprusside to the same extent produced large and significant increases in HR and RSNA in seven other renal hypertensive rats. Acute bilateral vagotomy was performed in seven of the declipped rats, which induced an immediate increase in MAP (+35 +/- 10 mmHg, P less than 0.05), HR +28 +/- 10 beats min-1, P less than 0.05) and RSNA (+51 +/- 19%, P less than 0.05). A few minutes afterwards the vagotomy pressure again started to fall and was, after another 90 min 107 +/- 10 mmHg together with slight reductions in HR and RSNA. Another group of six rats were initially exposed to bilateral vagotomy. In these vagotomized rats declipping also induced hypotension (204 +/- 10 to 95 +/- 7 mmHg, P less than 0.001), together with tendencies of decreases in HR (425 +/- 17 to 397 +/- 17 beats min-1) and in RSNA (-4 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1986

Peripheral haemodynamics after surgical reversal of two-kidney, one clip renal hypertension in rats.

The changes in peripheral haemodynamics and regional resistances were studied during the rapid fall in mean arterial pressure (MAP) after surgical reversal of two-kidney, one clip renal hypertension in rats (RHR). The controls used were sham-declipped RHR and normotensive control rats (NCR). During the 2 h following renal artery declipping or sham-operation, MAP and heart rate (HR) were followed continuously. Finally, the regional blood flows in the kidneys, small intestine and skeletal muscle were determined by the microsphere technique. Declipping caused MAP to fall from 167 +/- 5 to 108 +/- 5 mmHg (n = 10) with a concomitant fall in HR from 424 +/- 11 to 363 +/- 14 beats/min (P less than 0.01). The calculated vascular resistances fell in the intestinal and declipped renal vascular beds by 50-60% compared with sham-operated rats (P less than 0.01). However, vascular resistances remained unchanged in skeletal muscle and in the untouched kidney. This indicates that the reduction in flow resistance varies in the different vascular beds, presumably reflecting a mixture of suppressed sympathetic activity and direct vasodilatory actions induced by mechanisms activated upon reversal of two-kidney, one clip renal hypertension by renal artery declipping.

Animals↗
PubMed1984

Cardiovascular studies in rats with respect to some functional and structural relationships of relevance in hypertension and ordinary aging.

Five current lines of cardiovascular studies in rats are outlined, mainly dealing with some functional and structural relationships of particular relevance for hypertension and ordinary aging: 1. Characteristics of the smooth muscles and their neurogenic control in 'Windkessel' arteries, conduit arteries, precapillary resistance vessels and venous capacitance vessels from normotensive rats (WKY) with comparisons to rats with primary hypertension (SHR). 2. Different types of structural renovascular adaptation, comparing aging with advancing SHR hypertension, with 'high-pressure' and 'low-pressure' kidneys in one-clip, two-kidney renal hypertension, and with hypertrophied kidneys in uni-nephrectomized normotensive rats. 3. Relationships between 'structural autoregulation', wall distensibility, vascular reactivity and smooth muscle sensitivity in SHR and WKY hindquarter resistance vessels along with aging. 4. Relationships between wall thickness, luminal dimension and contractility in left ventricles from SHR and WKY during aging, and when one-clip, two-kidney hypertension is superimposed. 5. Interference with the capacity of the neurohormonal mechanisms counteracting blood loss in rats when on chronic low-salt diet.

Aging↗
PubMed1984

Suppression of the sympathetic nerve activity after surgical reversal of two-kidney, one clip hypertension in rats.

The change in tonic renal efferent sympathetic nerve activity (RSNA) was studied during the rapid fall in mean arterial pressure (MAP) after surgical reversal of two-kidney, one clip hypertension in rats (RHR). Controls used were intact RHR exposed to the same fall in MAP induced by slow infusion of sodium nitroprusside. Within 2 h after declipping, MAP had fallen from 191 +/- 9 mmHg to 106 +/- 8 mmHg. During this decline in pressure, the reflex increase in RSNA, ordinarily following a decrease in pressure, was clearly suppressed; after a short and transient initial increase, RSNA was below the control level. In comparison, upon vascular dilatation with sodium-nitroprusside, the same fall in MAP was accompanied by a 117 +/- 30% increase in RSNA (P less than 0.01). Thus, the rapid normalization of MAP after reversal of renovascular hypertension involves a mechanism that exerts a suppressive action on the efferent sympathetic activity.

Animals↗
PubMed1983

Age-dependent alterations in the structurally determined vascular resistance, pre- to postglomerular resistance ratio and glomerular filtration capacity in kidneys, as studied in aging normotensive rats and spontaneously hypertensive rats.

Maximally dilated renal vascular beds of 13-month-old NCR and SHR were compared to explore how aging respectively longstanding primary hypertension structurally alters total renal resistance, pre/postglomerular resistance ratio and maximal glomerular filtration capacity, as measured per unit kidney weight. According to comparisons of 1.5- and 3.5-month-old NCR and SHR (Folkow et al. 1977), a structurally increased pre/postglomerular resistance ratio rapidly resets the renal "longterm barostat function" in SHR to match the 30-40% pressure rise, thereby increasing total renal resistance 15-20%, while filtration capacity is unaltered so far. In NCR aging to 13 months hardly alters arterial pressure, but increases total renal resistance 10-15%, mainly affecting postglomerular vessels, while filtration capacity is reduced 25%. 13-month-old SHR show an additional 15% pressure rise and--relative to agematched NCR--a further 35% reduction of filtration capacity with a 30-35% increase of total renal resistance, which mainly affects the postglomerular vessels as the resistance ratio is now barely above that in NCR. Thus, advancing SHR hypertension seems to start a renal vicious circle, because accentuated reductions of filtration capacity are parallelled by structural postglomerular resistance increases apparently to maintain GFR by raised filtration pressure which, however, accelerates glomerular deterioration.

Aging↗
PubMed1983

"Structural autoregulation" of blood flow and GFR in the two renal vascular beds from two-kidney, one-clip renal hypertensive rats, as compared with kidneys from uni-nephrectomized and intact normotensive rats.

Both kidneys from two-kidney, one-clip renal hypertensive rats (RHR) and the hypertrophied kidney of uni-nephrectomized rats (UNR) were investigated during artificial perfusion with 2% Dextran solution and kerosene at maximal vasodilatation, and studied with respect to organ weight, vascular resistance, preglomerular/postglomerular resistance ratio and glomerular filtration capacity. Paired perfusions were throughout used, isolated kidneys from age-matched normotensive rats serving as controls. The untouched, "high-pressure" RHR kidney had increased 40% in weight/100 g b.w. while its vascular resistance at maximal dilatation had increased almost 60%/g organ weight. Glomerular filtration capacity and preglomerular/postglomerular resistance ratio remained, however, largely unchanged. The clipped "low-pressure", RHR kidney was reduced 40% in weight and 45% in renal vascular resistance/g organ weight. It also showed a reduced pre/postglomerular resistance ratio and some reduction of filtration capacity. The remaining hypertrophied kidney in UNR had increased 40% in weight, while its vascular resistance and filtration capacity/g organ weight, as well as its pre/postglomerular resistance ratio were unchanged. It is concluded that the kidney in renovascular hypertension rapidly adapts structurally not only in tissue mass, but also concerning total vascular resistance and pre/postglomerular resistance ratio, so as to chronically "autoregulate" GFR to match the altered pressure situation. Likewise, after unilateral nephrectomy the remaining, normotensive kidney increases in mass, with matched increases in blood flow and glomerular filtration capacity, while total resistance/g organ weight and the pre/postglomerular resistance ratio remain at normotensive levels.

Adaptation, Physiological↗
PubMed1983

Structurally based changes of renal vascular reactivity in spontaneously hypertensive and two-kidney, one-clip renal hypertensive rats, as compared with kidneys from uninephrectomized and intact normotensive rats.

Renal vascular beds from spontaneously hypertensive rats (SHR) at different stages of hypertension, from two-kidney, one-clip renal hypertensive rats (RHR) and from uninephrectomized rats (UNR) were in constant-flow, paired perfusions compared with kidneys from normotensive control rats (NCR) concerning vascular smooth muscle sensitivity to noradrenaline (NA) and resistance vessel reactivity, as reflected by the position, respectively the shape, of the dose-resistance response curves. None of these kidney variants differed significantly from controls concerning smooth muscle sensitivity to NA during in vitro perfusion. However, both the steepness and maximal pressor responses of the renal resistance curves increased progressively with age in SHR, to become ultimately much enhanced when related to age-matched controls. It suggests a well preserved smooth muscle contractility and a progressive elevation of the average wall/lumen ratio in the SHR renal resistance vessels. Also the untouched, "high-pressure" RHR kidneys showed increased vascular reactivity, while it was somewhat reduced in the clipped, "low-pressure" RHR kidneys and unchanged in the hypertrophied but normotensive UNR kidneys. These results, when combined with other findings concerning renal vascular design (Göthberg & Folkow 1982a), illustrate how the renal resistance vessels readily adapt structurally to hypertension, hypotension, kidney hypertrophy and also with age, and in directions which tend to chronically "autoregulate" glomerular blood supply and filtration.

Age Factors↗
PubMed1983

Response to slow, graded bleeding in salt-depleted rats.

The response to slow bleeding was studied in rats on low sodium intake (0.04%) versus 'ordinary' (0.4%) intake. After 12 days on the diets acute experiments were performed on paired, conscious rats. Initially the salt-depleted rats had slightly lower mean arterial pressure (121 +/- 2 versus 129 +/- 3 mmHg, n = 30 pairs, P less than 0.02). Heart rate (HR), cardiac output, plasma volume, extracellular volume and plasma renin activity (PRA) did not differ significantly, while haematocrit was slightly higher in the salt-depleted rats (46.5 +/- 0.3 versus 45.1 +/- 0.5%, P less than 0.05). The animals were then slowly bled 1 ml every 5 min until mean arterial pressure (MAP) fell and remained below 50 mmHg. The controls tolerated up to a 55 +/- 1% loss of initial blood volume, while the salt-depleted rats turned into irreversible shock already after losing 38 +/- 2% (P less than 0.001). At this stage compensatory haemodilution, HR and PRA increases were less pronounced than in the controls, suggesting that chronic sodium restriction had somehow interfered with the neurohormonal defences against accidental salt fluid losses.

Animals↗
PubMed1982

Sodium balance during development of hypertension in the spontaneously hypertensive rat (SHR).

Sodium balance was studied in 7 and 16 week old male spontaneously hypertensive rats (SHR), in matched normotensive Wistar rats (NCR) and in Wistar Kyoto rats (WKR). The animals were placed in metabolic cages and given diets with either normal sodium content (5.35 mmol sodium/100 g food) or with a sodium content 3 or 10 times the normal. Whether on normal or increased sodium diet we did not observe any increased sodium retention in either SHR age group. However, in both SHR groups urinary sodium excretion was correspondingly increased compared with the controls. This shift of sodium excretion from kidneys to gastrointestinal tract in SHR did not reflect any 'primary' inability of the SHR kidneys to excrete sufficient sodium amounts since on high sodium diet they excreted the increased sodium load as readily as the normotensive controls. The present results do not support the concept that a primary renal retention of sodium and water should be of pathogenetic importance for the SHR variant of primary hypertension.

Age Factors↗
PubMed1980

Studies on the role of sodium-potassium-activated ATPase as determinant of vascular reactivity in Wistar-Kyoto and spontaneously hypertensive rats.

1. The role of Na+-K+-activated ATPase in the regulation of resistance vessel reactivity to barium chloride and noradrenaline was investigated with a pair-perfused hindquarter technique in spontaneously hypertensive rats and Wistar-Kyoto rats (6 and 12 week old). Ouabain (10(-4) mol/l) was used to inhibit the sodium pump. 2. In all groups studied, dose-response curves to agonists were shifted to the left when ouabain was added to the perfusion medium. This potentiation in vascular reactivity produced by ouabain was expressed as 'index for sodium-pump inhibition' (ISPI = ED 50 of an agonist/ED50 + ouabain). 3. In mature rats index for sodium-pump inhibition calculated for both agonists was significantly greater in spontaneously hypertensive rats in comparison with Wistar-Kyoto rats, but not so in young spontaneously hypertensive rats. There was, however, a trend towards increased noradrenaline sensitivity in spontaneously hypertensive rats although the difference from Wistar-Kyoto rats was not statistically significant. 4. The data may suggest that there is some increase in the activity of the sodium pump in the resistance vessels of mature spontaneously hypertensive rats, perhaps to compensate for an increased passive sodium permeability.

Animals↗