Search PubMed⌕ Search

Biomedical subjects

S Lundin

Publications and source records attributed to S Lundin.

At least 145 records · Page 8Linked to original sources

Interaction between "mental stress" and baroreceptor reflexes concerning effects on heart rate, mean arterial pressure and renal sympathetic activity in conscious spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) were compared concerning the interactions between cortico-hypothalamic alerting responses and baroreflex influences on neurogenic cardiovascular control. For this purpose mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were continuously recorded during night time in conscious, otherwise undisturbed rats. Baroreceptor sensitivity was assessed as percentage HR and RSNA reductions per mmHg MAP elevation when a standardized phenylephrine infusion was performed. A state of acute "mental stress" could be induced by a likewise standardized sudden blowing of air. These two opposing influences on neurogenic cardiovascular control were also experimentally superimposed in various ways and the effects on MAP, HR and RSNA followed. During "rest" RSNA was higher in SHR than in WKY and it also increased more during "mental stress". The baroreflex sensitivity was clearly reduced in SHR and WKY concerning HR reduction (0.44 +/- 0.06 vs. 0.78 +/- 0.08%/mmHg; p less than 0.01) but not so concerning RSNA, which was similar in SHR and WKY (2.6 +/- 0.2 vs. 2.9 +/- 0.4%/mmHg). If expressed (HR + 1 +/- 3%; p less than 0.025 vs. SHR and RSNA + 11% +/- 10, p less than 0.01 vs. SHR). These results) (0.10 +/- 0.02 vs. 0.06 +/- 0.01 microV/mmHg; p less than 0.12). Also single fibre recordings in anaesthetized rats showed the same principle difference between SHR and WKY.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Spontaneous variations in arterial blood pressure, heart rate and sympathetic nerve activity in conscious normotensive and spontaneously hypertensive rats.

In the present study we have recorded spontaneous variations in mean arterial blood pressure (MAP), heart rate (HR) and mean rectified splanchnic nerve activity (SNA) in conscious undisturbed normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The variability in blood pressure was not significantly different but HR variability tended to be lower in SHR. The variability in SNA expressed as % change from mean value was not significantly different between SHR and WKY. By computer techniques the correlation between HR, MAP and SNA could be calculated during spontaneous variations of these parameters. The slope of the regression line correlating HR and SNA was significantly steeper in SHR than in WKY (0.73, 0.47 resp.). Thus a certain change in HR was associated by a greater change in SNA in SHR compared with WKY. Spontaneous changes in SNA could be divided in principally two different patterns. One typical pattern was a rise in SNA in parallel with a drop in MAP. This pattern was most likely triggered by the arterial baroreceptors and was called a "baroreceptor-pattern". Marked spontaneous excitations in SNA and HR was also observed during natural behaviours such as eating, drinking and explorative behaviour, a so called "centrally mediated pattern".

Animals↗

Prescriptive authority for nurse practitioners: a comparative study of professional attitudes.

We assessed the attitudes of Wyoming physicians, pharmacists, nurses, and nurse practitioners about granting prescriptive authority to nurse practitioners. Support for the issue was mixed, with physicians expressing the strongest disagreement. All groups supported limitation of authority to a specific drug formulary, collaborative regulation, and mandatory certification and continuing education if prescriptive authority is granted to nurse practitioners.

Attitude of Health Personnel↗

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↗

Diastolic properties of the hypertrophied left ventricle in spontaneously hypertensive rats.

The influence of myocardial hypertrophy on left ventricular volume compliance was studied in vitro in isolated hearts of 4 and 19 month old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). In both SHR groups diastolic volume compliance was similar to that in the controls, despite the presence of left ventricular hypertrophy. This seems to be mainly due to an altered geometric situation, since with increased wall thickness to internal radius ratio (w/ri), which was at hand, the less are outer myocardial layers stretched at a given increase in ventricular volume. This may imply that these layers will only little interfere with luminal distension (and thereby with diastolic volume compliance) in SHR. It was also observed that the progressive increase of ventricular hypertrophy from 4 to 19 months of age did not further increase w/ri in SHR, indicating an increase in overall ventricular size with age. Left ventricular end diastolic pressure (LVEDP) was also measured in conscious 5 week and 4 month old SHR compared with matched controls. LVEDP increased with the development of hypertension and was significantly elevated in 4 month old SHR. This will increase also the average diastolic pre-stretch of the SHR left ventricle and mobilize the "Starling mechanism" to maintain a normal stroke volume against the increased afterload for the heart in established hypertension. This seems particularly important since the hypertrophic w/ri increase (about 20%) is smaller than the great elevation of mean arterial pressure (40-50%) in SHR.

Age Factors↗

Renal denervation and sodium balance in young spontaneously hypertensive rats.

In 7-week-old male, spontaneously hypertensive rats (SHR) and matched normotensive control rats, Wistar Kyoto Rats (WKY), a bilateral renal denervation was performed. In two additional groups of rats a sham denervation was done (SHRS, WKYS). The animals were then kept in metabolic cages during a 10-day period during which sodium intake, urine volume, urinary sodium excretion, fecal sodium excretion, urinary aldosterone excretion and plasma renin activity were determined. Fractional urinary excretion of sodium was higher in the denervated SHR (p less than 0.1) and WKY (p less than 0.05) during the first 3 days after denervation, but during the following 3-day periods no difference between denervated and sham-operated groups was noted. The difference in fractional urinary excretion of sodium initially was due to a diminished urinary sodium excretion in the sham-operated groups since both SHRS and WKYS exhibited a significant increase between the first and the last 3-day period. Urine volume increased significantly in both SHR and WKY after denervation. Urinary aldosterone excretion on the 7th day after denervation was significantly lower in SHR compared to WKY, but there was no significant difference between the denervated and sham-operated groups. PRA was also significantly lower in SHR but no significant decrease was seen after denervation.

Aldosterone↗

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↗

Interaction between mental stress and baroreceptor control of heart rate and sympathetic activity in conscious spontaneously hypertensive (SHR) and normotensive (WKY) rats.

Spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY) were compared with regard to the interaction between cortico-hypothalamic alerting responses and the baroreflex influences on neurogenic cardiovascular control. Baroreceptor sensitivity was assessed as heart rate (HR) and renal sympathetic nerve activity (RSNA) reduction per mmHg mean arterial pressure (MAP) increase by phenylephrine infusion. Response to 'mental stress' was studied. Addition of 'mental stress' during baroreceptor activation (30 mmHg MAP increase) was also performed. RSNA was higher in SHR than in WKY during rest and increased more during stress. Baroreflex sensitivity was reduced in SHR compared with WKY concerning HR (0.44 +/- 0.06 versus 0.78 +/- 0.08%/mmHg). Percentage RSNA reduction was similar, while RSNA reduction appeared greater in SHR in comparison with WKY (0.10 +/- 0.02 and 0.06 +/- 0.01 microV/mmHg, P less than 0.12). During baroreflex activation 'mental stress' increased both HR (+24 +/- 7%) and RSNA (+114 +/- 21%) in SHR with almost no changes in WKY. The results suggest an increased cortico-hypothalamic activity in SHR, which is clearly augmented during 'mental stress' and readily overcomes baroreflex inhibitory influences on sympathetic activity.

Animals↗

Left ventricular hypertrophy improves cardiac performance in spontaneously hypertensive rats.

Cardiac function was studied in spontaneously breathing, adult spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY). By rapid intravenous blood infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke infusion, the relation between left ventricular end-diastolic pressure (LVEDP) and stroke volume (SV) was determined while the cardiac nervous control was pharmacologically blocked. Since SV is greatly influenced by the level of afterload (mean arterial pressure, MAP), SV was also determined at increased MAP (constriction of abdominal aorta) and at decreased MAP (vasodilation by hydralazine). At low LVEDP levels, a rightward shift of the Frank-Starling relationship was observed in SHR. This rightward shift seems mainly to depend on the increased MAP present in SHR since it was less prominent if MAP was lowered to normotensive levels in SHR. Maximal SV during volume infusion was similar in SHR and WKY, despite a much higher MAP in SHR. When peak SV was instead compared at similar MAP levels for both (either at normotensive' or 'hypertensive' levels) it was always significantly greater in SHR, and was increased largely in proportion to their increased left ventricular weight. This indicates that the left ventricular hypertrophy present in SHR is, at least at this stage, a physiological adaptation of the heart to increase its performance, in order to maintain a normal SV and hence cardiac output, despite an increased arterial pressure.

Animals↗

Renal function and sympathetic activity during mental stress in normotensive and spontaneously hypertensive rats.

The aim of the present study was to explore the role of the renal sympathetic nerves in the urinary sodium excretion response to 'mental stress' in spontaneously hypertensive rats (SHR). In conscious male SHR and male Wistar Kyoto rats (WKY) urinary sodium excretion and renal function were measured both during 'rest' and during a 20 min period of 'mental stress'. Experiments were also performed on renal denervated rats. In addition, renal sympathetic activity was measured in a separate group of rats. Urinary sodium excretion, similar at rest in SHR and WKY, decreased significantly more during the stress period in SHR (-64 +/- 5%) than in WKY (-34 +/- 7%), despite a greater arterial pressure increase in SHR. Renal sympathetic nerve activity which already at rest was higher in SHR than in WKY, also increased much more in SHR during stress than in WKY. The more intense renal sympathetic activation during stress may explain the greater reduction in urinary sodium excretion in SHR, because renal denervation almost abolished this latter response. Thus, during 'mental stress' the increased renal sympathetic activity reduces urinary sodium excretion in SHR despite the pressure rise, perhaps explaining why renal denervation delays the rise in arterial pressure in young SHR. The tachycardia response in SHR gradually subsided towards the end of the stress period, while renal sympathetic activity remained elevated. This indicates that neurogenic heart rate increases if anything underestimate the extent of sympathetic activation to e.g. the renal and splanchnic regions during increased alertness.

Animals↗

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↗

Hormonal pattern during development of hypertension in spontaneously hypertensive rats (SHR).

Urinary excretion of sodium, noradrenaline, dopamine, aldosterone, prostaglandin E2 and plasma renin activity were determined in 7 and 16 weeks old spontaneously hypertensive rats (SHR) and in two normotensive control strains, ordinary Wistar control rats (NCR) and Wistar-Kyoto normotensive rats (WKR). Each group consisted of 10-11 rats. The animals were kept in metabolic cages. Experiments were performed on standard diet (5-8 mmol Na+/100 g food) and with an increased (15.6 and 56.0 mmol Na+/100 g food) salt intake. At 7 weeks of age, when SHR are in a borderline phase of hypertension, they exhibited a decreased urinary sodium excretion, and an increased urinary noradrenaline excretion compared to controls. The latter might reflect an increased overall activity of the sympathetic nervous system. Urinary dopamine excretion was also increased probably mirroring a higher activity in a renal natriuretic dopamine system. Plasma renin activity and urinary aldosterone excretion were depressed. At 16 weeks of age, when SHR are in an early establishment phase of hypertension, urinary sodium excretion was still lower in SHR, while urinary noradrenaline and dopamine excretions had become normal compared to controls. Plasma renin activity and urinary aldosterone excretion remained depressed. Urinary PGE2 excretion, only determined in this age group, was significantly higher in SHR.

Aldosterone↗

Intra-erythrocyte sodium and (Na+,K+-activated)-ATPase concentration and urinary aldosterone excretion in spontaneously hypertensive rats.

1. Intra-erythrocyte sodium, potassium, ATP and (Na+,K+-activated)-ATPase concentrations and urinary aldosterone excretion were compared in 3-month-old spontaneously hypertensive rats (n = 11) and normotensive Wistar-Kyoto control rats (n = 11). 2. Spontaneously hypertensive rats exhibited significantly higher intra-erythrocyte sodium concentration (5.5 +/- 1.3 vs 4.0 +/- 1.1 mmol/l of erythrocytes, P less than 0.01). No significant difference was found in intra-erythrocyte potassium. ATP or (Na+,K+-activated)-ATPase concentration. 3. Mean urinary aldosterone excretion was significantly lower in spontaneously hypertensive rats (66.3 +/- 6.5 pmol/24 h) than in Wistar-Kyoto rats (90.5 +/- 10.6 pmol/24 h, P less than 0.01). No significant relationship between urinary aldosterone and intra-erythrocyte sodium concentration was found in spontaneously hypertensive or Wistar-Kyoto rats or in the pooled group. 4. These results are thus consistent with previous findings of an increased intracellular sodium concentration in spontaneously hypertensive rats, but do not support the hypothesis that aldosterone is a dominant regulator of intracellular sodium concentration.

Adenosine Triphosphate↗

Left ventricular hypertrophy improves cardiac function in spontaneously hypertensive rats.

1. The influence of different arterial pressures on the relationship between diastolic filling pressure and stroke volume was studied during pharmacological cardiac nerve blockade in adult, anaesthetized spontaneously hypertensive rats in comparison with matched normotensive Wistar--Kyoto rats. 2. Peak stroke volumes, obtained by rapid blood volume expansion were similar in both types of rat, despite a more than 40% higher mean arterial pressure in the spontaneously hypertensive rats. 3. When peak stroke volumes were compared in the two groups at equal 'normotensive' or 'hypertensive' arterial pressures, they were always greater in the spontaneously hypertensive rats. 4. Calculation of diastolic wall/lumen ratios indicated that the increase of maximal stroke work in the spontaneously hypertensive rats closely matched the hypertrophic increase in wall/lumen ratio of the left ventricle. 5. These results indicate that left ventricular hypertrophy in established primary hypertension is a physiological adaptation to match left ventricular performance to the raised afterload.

Animals↗