Preload does not affect relaxation rate in normal, hypoxic, or hypertrophic myocardium

1990 ◽  
Vol 258 (1) ◽  
pp. H191-H197 ◽  
Author(s):  
M. R. Zile ◽  
C. H. Conrad ◽  
W. H. Gaasch ◽  
K. G. Robinson ◽  
O. H. Bing
Keyword(s):  
Relaxation Rate ◽  
Isometric Force ◽  
Muscle Length ◽  
Independent Effect ◽  
Shr Rats ◽  
Spontaneously Hypertensive ◽  
Maximum Isometric Force ◽  
Hypertrophic Myocardium ◽  
Wistar Kyoto ◽  
Tension Curves

To determine whether isolated changes in preload (end-diastolic force) can influence myocardial relaxation rate in normal or abnormal (hypoxic or hypertrophic) hearts, isolated LV papillary muscles from normal Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats were studied using physiologically sequenced contractions. While total (systolic) load and late (lengthening) load were held constant, maximum isometric force decline (peak -dT/dt) and maximum isotonic lengthening rate (peak +dL/dt) were measured at seven levels of preload that varied from 115 to 55% of the resting tension at maximum length-tension curves (Lmax). Muscles from normal rats were studied in the oxygenated state (95% O2-5% CO2) and in the hypoxic state (95% N2-5% CO2). Preload did not effect peak -dT/dt or peak +dL/dt in either oxygenated or hypoxic muscles. During hypoxia, peak -dT/dt and peak +dL/dt were 9.5 +/- 1.0 g.mm-2.s-1 and 0.3 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 9.0 +/- 1.2 g.mm-2.s-1 and 0.2 +/- 0.1 at a preload of 55%. In separate experiments, the effect of preload on relaxation rate was studied in WKY and SHR rats. In neither group did preload have an independent effect on relaxation rate. In the SHRs, peak -dT/dt and peak +dL/dt were 24.3 +/- 5.3 g.mm-2.s-1 and 0.7 +/- 0.1 muscle length/s, respectively, at a preload of 115% compared with 24.7 +/- 6.6 and 0.8 +/- 0.1 at a preload of 55%. Thus, in hypoxic and hypertrophic myocardium, as in normal muscle, an acute isolated change in preload did not influence the rate of force decline or muscle lengthening.

Altered aortic reactivity and lowered blood pressure associated with high calcium intake

1986 ◽  
Vol 251 (5) ◽  
pp. H976-H983 ◽  
Author(s):  
R. D. Bukoski ◽  
D. A. McCarron
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Isometric Force ◽  
Control Diet ◽  
Shr Rats ◽  
High Calcium Intake ◽  
Spontaneously Hypertensive ◽  
Aortic Smooth Muscle ◽  
High Calcium ◽  
Wistar Kyoto

The hypothesis that dietary calcium (dCa) alters functional properties of aortic smooth muscle in the spontaneously hypertensive rat (SHR) was tested. At 6 wk of age, Wistar Kyoto (WKY) and (SHR) rats were placed on a control diet containing 1% Ca. The experimental SHR group received a 2%-calcium diet. After an average of either 8 or 15 wk on the diets (WOD), aortic rings were prepared for measurement of passive elastic properties and isometric force development. Differences in blood pressure (BP) were not apparent until after 8 WOD when the BP of SHRs on 2% dCa were 10-15 mmHg lower than SHRs on 1% dCa (P less than 0.05). After 8 WOD, when the BP effect first emerged, no significant differences in aortic properties were observed between the SHR groups. However, after 15 WOD, aortas of SHRs on 2% dCa were more compliant than those of SHRs on 1% dCa and between 8 and 15 WOD the sensitivity to KCl decreased in aortas from the WKY group and the SHRs on 2% dCa, but not the SHR-1% dCa group (mean effective dose went from 14.4 +/- 0.4 to 18.5 +/- 0.9 mM for WKY and from 13.6 +/- 0.6 to 17.1 +/- 1.2 mM for SHRs on 2% dCa, P less than 0.05). In addition, between 8 and 15 WOD, a significant decrease in response to a calcium (Ca2+) challenge after removal of K+ and Ca2+ occurred in aortas of the SHRs on 2% dCa, but not in the control diet groups, indicating that a decrease in aortic reactivity was present in the Ca2+-supplemented SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Contractile responses to ouabain and K+-free solution in aorta from hypertensive rats

1986 ◽  
Vol 250 (4) ◽  
pp. H612-H619 ◽  
Author(s):  
R. S. Moreland ◽  
T. C. Major ◽  
R. C. Webb
Keyword(s):  
Channel Blocker ◽  
Isometric Force ◽  
Maximal Response ◽  
Na Channel ◽  
Free Solution ◽  
Contractile Responses ◽  
Spontaneously Hypertensive ◽  
Force Development ◽  
Monensin A ◽  
Wistar Kyoto

This study characterizes isometric force development in response to ouabain and K+-free solution in isolated aortic strips from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. SHR aortas were more sensitive to ouabain than those from WKY (threshold: SHR, 3.1 X 10(-5) M; WKY, 25.6 X 10(-5) M), and force development in response to 10(-3) M ouabain was greater in SHR (SHR, 586 +/- 51 mg; WKY, 245 +/- 24 mg). Monensin, a Na+ ionophore, potentiated contractile responses to ouabain, whereas amiloride, a Na+ channel blocker, and low Na+ solutions depressed contractile responses to ouabain. Contractile responses of SHR aortic strips to K+-free solution were faster than those of WKY aortic strips [time to half-maximal response (t1/2): SHR, 24 +/- 5 min; WKY, 47 +/- 4 min]. Maximal force development by aortic strips from SHR in response to K+-free solution was not different from that of WKY aortic strips (SHR, 808 +/- 34 mg; WKY, 750 +/- 37 mg). Monensin (10(-5) M) increased the rate of force development to K+-free solution to a greater extent in WKY aortic strips than in those from SHR (t1/2: SHR, 3 +/- 1 min; WKY, 4 +/- 2 min). Amiloride and low Na+ solution depressed contractile responses to K+-free solution in both SHR and WKY aortic strips. These observations demonstrate that SHR aortas are more responsive to ouabain and K+-free solution compared with WKY aortas. Contractile responses to ouabain and K+-free solution were sensitive to experimental interventions that alter transmembrane Na+ movements.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension in SHR rats: contribution of maternal environment

1987 ◽  
Vol 253 (4) ◽  
pp. H980-H984 ◽  
Author(s):  
M. A. Cierpial ◽  
R. McCarty
Keyword(s):  
Shr Rats ◽  
Maternal Environment ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Rearing Conditions ◽  
Blood Pressures ◽  
Wistar Kyoto ◽  
Male Subjects ◽  
Cross Fostering

The role of the maternal environment in the development of hypertension in spontaneously hypertensive (SHR) rats was evaluated using the technique of reciprocal cross fostering. Litters of SHR and Wistar-Kyoto (WKY) normotensive pups were either reared by their natural mothers, in fostered to mothers of the same strain, or cross fostered to mothers of the opposite strain shortly after birth. Litters were weaned at 21 days of age, at which time all pups were weighed. At 18-20 wk of age, resting mean arterial blood pressures (MAP) and heart rates were determined for male subjects from the six groups (2 strains X 3 rearing conditions) via an indwelling tail artery catheter. At weaning, SHR animals weighed less than WKY animals. SHRs fostered to WKY mothers were significantly heavier than control SHRs, and WKYs fostered to SHR mothers were significantly lighter than WKY controls at weaning. These body weight differences were also evident in adulthood. Cross fostering SHR pups to normotensive WKY mothers resulted in a dramatic reduction in resting MAP measured in adulthood. Conversely, cross fostering WKY pups to SHR mothers had no measurable effect on adult resting MAP. We propose that an interaction between characteristics of the SHR maternal environment and a genetic susceptibility in SHR pups is essential in triggering the full expression of the hypertensive phenotype in this animal model of human essential hypertension.

Further analysis of cell membrane changes in genetic hypertension in rats by diphenylhexatriene fluorescence polarization

1984 ◽  
Vol 66 (6) ◽  
pp. 717-723 ◽  
Author(s):  
I. Aracon-Birlouez ◽  
T. Montenay-Carestier ◽  
M. A. Devynck
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Erythrocyte Membranes ◽  
Shr Rats ◽  
Erythrocyte Ghosts ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive ◽  
Platelet Membranes ◽  
Wistar Kyoto ◽  
Membrane Changes

1. Fluorescence Dolarization of dbhenvlhexa-triene embedded in membranes was used as an index of ‘microviscosity’ in platelets and ervthro—cyte ghosts of spontaneously hypertensive rats of the Okamoto-Aoki strain (SHR), Wistar-Kyoto strain (WKY) and of the hypertension-prone and -resistant Sabra strains (SBH and SBN), and the original Sabra strain (SB). 2. Microviscosity was increased both in erythrocyte ghosts and platelet membranes of male but not female SHR rats compared with WKY rats and in hypertension-prone Sabra rats compared with the original Sabra rats. 3. Acute and chronic salt loading increased the microviscosity of platelet membranes in all strains of rats but had no effect on the erythrocyte membranes. 4. Microviscosities of vesicles made of lipids extracted from SHR and WKY erythrocyte ghosts were similar. This supports the hypothesis that membrane proteins play a major role in the differences in microviscosity observed in SHR rats.

A bladder contractility constant

1983 ◽  
Vol 245 (5) ◽  
pp. R673-R677
Author(s):  
J. C. Byrne ◽  
A. Tozeren
Keyword(s):  
Initial Velocity ◽  
Active Component ◽  
Isometric Force ◽  
Muscle Length ◽  
Rate Of Change ◽  
Contractile Element ◽  
Tetanic Contraction ◽  
Muscle Contractility ◽  
Maximum Isometric Force ◽  
The Moment

Muscle contractility can be characterized by two related properties: force and velocity. The initial velocity of a tetanic contraction is inversely related to preload. This was demonstrated experimentally by Hill and quantified in his well-known empiric equation. Subsequent investigators argued that a theoretical maximum contractile element velocity (V max) could be predicted from the rate of change of isometric force. V max has been applied clinically in heart studies, prompting others to use similar methods to evaluate bladder contractility. These attempts have so far been unsuccessful. The present study shows for whole canine bladders that the time to reach maximum isometric force from the moment of onset of active contraction is a constant independent of muscle length, preload, and maximum force. This can be expressed as a frequency constant (omega) whose calculation appears similar to that for V max. In contrast to V max, omega is obtained only from the active component of pressure.

Isotonic relaxation in cardiac muscle

1975 ◽  
Vol 229 (3) ◽  
pp. 646-651 ◽  
Author(s):  
JE Strobeck ◽  
AS Bahler ◽  
EH Sonnenblick
Keyword(s):  
Cardiac Muscle ◽  
Isometric Force ◽  
Muscle Length ◽  
Constant Load ◽  
Papillary Muscles ◽  
Initial Length ◽  
Total Load ◽  
Relaxation Velocity ◽  
Force Velocity ◽  
Maximum Isometric Force

The force-velocity-length determinants of isotonic relaxation were studied in 12 cat papillary muscles. Isotonic relaxation velocity (VL) was found to be a function of total load (preload + afterload), with peak VL increasing to a maximum at loads approximately .3 to .4 Po(L') (Po(L') defined as maximum isometric force developed during a twitch at the experimental length) and falling with increasing loads. Initial muscle length (ML) had no effect on the peak VL with constant load. Increasing the initial length at which isotonic relaxation occurred (LL) decreased peak VL but did not alter the unique length-velocity trajectory at constant load. This unique length-velocity trajectory occurred, despite a wide variation in time during the contraction when peak VL was measured. Increasing Ca++ from 2.5 to 7.5 mM increased peak VL (1.73 +/- .16 to 2.32 +/- .20 ML/s) and shifted the entire length-velocity trajectory toward higher velocities of lengthening. The addition of 10 mM caffeine increased peak VL also (1.67 +/- .18 to 2.54 +/- .20 ML/s) and had a similar effect on the length-velocity trajectory during lengthening as Ca++. Both increased Ca++ and caffeine (10 mM) augmented the maximum VL measured on addition of load.

Length-dependent sensitivity of vascular smooth muscle in normotensive and hypertensive animals

1987 ◽  
Vol 253 (2) ◽  
pp. H402-H411 ◽  
Author(s):  
E. Coskinas ◽  
J. M. Price
Keyword(s):  
Muscle Length ◽  
Rat Aorta ◽  
Maximum Force ◽  
Anterior Tibial Artery ◽  
Response Curves ◽  
Spontaneously Hypertensive ◽  
Tibial Artery ◽  
Anterior Tibial ◽  
Norepinephrine Dose ◽  
Wistar Kyoto

Ring segments were obtained from the aorta of spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), and Wistar (WST) rats and from the anterior tibial artery of normotensive and hypertensive dogs. Norepinephrine dose-response curves were generated at lengths relative to that for maximum force (Lmax) and at a specific preload (in grams). The doses of stimulus necessary to elicit 10 and 50% maximum force of contraction (ED10 and ED50) are greater at lengths less than Lmax than at Lmax for all groups. When SHR rings are compared with WKY or WST rings, ED10 or ED50 is the same at either length. The same result was found in comparing normal and hypertensive dogs. ED10 and ED50 from hypertensive groups were the same as their respective control groups when compared at the same preload. We conclude that sensitivity of the rat aorta and dog anterior tibial artery to norepinephrine depends on muscle length, this relationship is not altered in hypertension, and the conclusion on sensitivity in hypertension is the same for excised rings compared at the same length or at the same preload. Contractility (active stress) was lower (rats) or the same (dogs) but thickness was greater in the hypertensive groups than in their controls. The results show that a change in the vessel wall that can cause increased flow resistance and pressure is not in sensitivity or contractility but in wall thickness. Apparent differences in sensitivity from normal and hypertensive animals can be explained by an unchanged length-dependent sensitivity. The results also show that differences in body weight will affect a comparison of wall tension but not of sensitivity.

scholarly journals Effect of a methionine-supplemented diet on the blood pressure of Wistar–Kyoto and spontaneously hypertensive rats

2003 ◽  
Vol 89 (4) ◽  
pp. 539-548 ◽  
Author(s):  
Sophie Robin ◽  
Véronique Maupoil ◽  
Frédérique Groubatch ◽  
Pascal Laurant ◽  
Alain Jacqueson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Homocysteine ◽  
Shr Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Complex Interactions ◽  
Methionine Concentration ◽  
Wistar Kyoto

The objectives of the present work were to evaluate the effect of a methionine-supplemented diet as a model of hyperhomocysteinaemia on the systolic blood pressure (BP) and vasomotor functions of aortic rings in Wistar–Kyoto (WKY) and spontaneously hypertensive rats (SHR). WKY and SHR rats, randomised into four groups, were fed a normal semisynthetic diet or a methionine (8 g/kg)-supplemented diet for 10 weeks. Systolic BP was measured non-invasively. At the end of the experiment, plasma homocysteine, methionine, cysteine and glutathione levels were determined. Vasoconstriction and vasodilatation of aortic rings were measured. The methionine-supplemented diet induced a significant increase in plasma homocysteine and methionine concentration in both WKY and SHR rats, an increase in plasma cysteine concentrations in WKY rats and an increase in the glutathione concentration in SHR. The systolic BP of WKY rats fed the methionine-supplemented diet increased significantly (P<0·01), whereas systolic BP was reduced in SHR. An enhanced aortic responsiveness to noradrenaline and a decreased relaxation induced by acetylcholine and bradykinin were observed in the WKY rats fed the methionine-enriched diet. In SHR, the bradykinin-induced relaxation was reduced, but the sodium nitroprusside response was increased. In conclusion, a methionine-enriched diet induced a moderate hyperhomocysteinaemia and an elevated systolic BP in WKY rats that was consistent with the observed endothelial dysfunction. In SHR, discrepancies between the decreased systolic BP and the vascular alterations suggest more complex interactions of the methionine-enriched diet on the systolic BP. Further investigations are needed to understand the paradoxical effect of a methionine-rich diet on systolic BP.

scholarly journals Perindoprilat Changes ANG (1-9) Production in Renal Arteries Isolated From Young Spontaneously Hypertensive Rats After ANG I Incubation

2016 ◽  
pp. 561-570
Author(s):  
P. P. WOŁKOW ◽  
B. BUJAK-GIŻYCKA ◽  
J. JAWIEŃ ◽  
R. OLSZANECKI ◽  
J. MADEJ ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Renal Artery ◽  
Spontaneously Hypertensive Rats ◽  
Renal Arteries ◽  
Ang Ii ◽  
Shr Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Old Rats ◽  
Wistar Kyoto

We used mass spectrometry to quantitate production of angiotensinogen metabolites in renal artery of 3- and 7-month-old Wistar-Kyoto (WKY) and Spontaneously Hypertensive Rats (SHR). Tissue fragments were incubated for 15 min in oxygenated buffer, with added angiotensin I. Concentrations of angiotensins I (ANG I), II (ANG II), III (ANG III), IV (ANG IV), angiotensin (1-9) [ANG (1-9)], angiotensin (1-7) [ANG (1-7)], and angiotensin (1-5) [ANG (1-5)], excreted into the buffer during experiment, were measured using liquid chromatography-mass spectrometry (LC/MS) and expressed per mg of dry tissue. Effects of pretreatment with 10 μM perindoprilat on the production of ANG I metabolites were quantitated. Background production of any of ANG I metabolites differed neither between WKY and SHR rats nor between 3- and 7-month-old rats. Perindoprilat pretreatment of renal arteries resulted, as expected, in decrease of ANG II production. However, renal arteries of 7-month-old SHR rats were resistant to ACE inhibitor and did not change ANG II production in response to perindoprilat. In renal arteries, taken from 3-month-old rats, pretreated with perindoprilat, incubation with ANG I, resulted in the level of ANG (1-9) significantly higher in SHR than WKY rats. Our conclusion is that in SHR rats, sensitivity of renal artery ACE to perindoprilat inhibition changes with age.

Supraspinatus Muscle Architecture and Physiology in a Rabbit Model of Tenotomy and Repair

2021 ◽  
Author(s):  
Sydnee A. Hyman ◽  
Isabella T. Wu ◽  
Laura S. Vasquez-Bolanos ◽  
Mackenzie B. Norman ◽  
Mary C. Esparza ◽  
...  
Keyword(s):  
Rotator Cuff ◽  
Isometric Force ◽  
Rabbit Model ◽  
Muscle Length ◽  
Peak Stress ◽  
Structural Data ◽  
Rotator Cuff Tears ◽  
Time Data ◽  
Maximum Isometric Force ◽  
Over Time

Chronic rotator cuff tears can cause severe functional deficits. Addressing the chronic fatty and fibrotic muscle changes is of high clinical interest; however, the architectural and physiological consequences of chronic tear and repair are poorly characterized. We present a detailed architectural and physiological analysis of chronic tear and repair (both over 8 and 16 weeks) compared to age-matched control rabbit supraspinatus (SSP) muscles. Using female New Zealand White Rabbits (N=30, n=6/group) under 2% isofluorane anesthesia, the SSP was surgically isolated and maximum isometric force measured at 4-6 muscle lengths. Architectural analysis was performed, and maximum isometric stress was computed. Whole muscle length-tension curves were generated using architectural measurements to compare experimental physiology to theoretical predictions. Architectural measures are consistent with persistent radial and longitudinal atrophy over time in tenotomy that fail to recover after repair. Maximum isometric force was significantly decreased after 16 wks tenotomy and not significantly improved after repair. Peak isometric force reported here are greater than prior reports of rabbit SSP force after tenotomy. Peak stress was not significantly different between groups and consistent with prior literature of SSP stress. Muscle strain during contraction was significantly decreased after 8-wks of tenotomy and repair, indicating effects of tear and repair on muscle function. The experimental length-tension data was overlaid with predicted curves for each experimental group (generated from structural data), exposing the altered structure-function relationship for tenotomy and repair over time. Data presented here contribute to understanding the physiological implications of disease and repair in the rotator cuff

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