Physical and electrocardiographic evaluation of horses used for wagon traction / Avaliação física e eletrocardiográfica de cavalos utilizados para tração de carroças

The objective of this research was to evaluate the electrocardiogram (ECG) of horses used for wagon traction and to compare the results with the parameters obtained from inactive horses or horses submitted to a training routine. Fifty-six 3-15-year-old healthy horses (22 females and 34 males) were divided into three groups: control (without a work routine; N=21), wagon traction (N=25) and athlete (N=10) and submitted to physical examination and ECG (at rest). The rhythm, heart rate (HR), amplitude and duration of ECG waveforms and intervals were obtained from the frontal plane and base-apex leads. Heart score (HS) was calculated using the arithmetic mean of QRS duration in LI, LII and LIII. Measurements of ECG waves were smaller in control group, in comparison with wagon traction and athlete groups, suggesting that exercise can change ECG. Similar results were observed in the wagon traction and athlete groups, but the electrophysiological adjustments to exercise were not the same for these groups.(AU)

O objetivo deste trabalho foi avaliar o eletrocardiograma (ECG) de cavalos que tracionavam carroças (carroceiros; N=25), comparando os resultados com os parâmetros de cavalos que não realizavam essa atividade (controles; N=21), ou que apresentavam uma rotina de treinamento (atletas; N=10). O ECG foi precedido pelo exame físico do animal e, a partir das derivações no plano frontal e na base-ápice, determinou-se o ritmo, a frequência cardíaca, a amplitude e a duração das ondas e dos intervalos, em repouso. O escore cardíaco foi calculado pela média aritmética da duração do complexo QRS em DI, DII e DIII. O grupo controle apresentou menores valores de amplitude e duração das ondas do ECG, em comparação aos grupos carroceiro e atleta, sugerindo que o exercício pode alterar o ECG. Resultados semelhantes foram observados nos grupos carroceiro e atleta; contudo, os ajustes eletrofisiológicos ao exercício não foram os mesmos para esses dois grupos.(AU)

Action of ANP on the nongenomic dose-dependent biphasic effect of aldosterone on NHE1 in proximal S3 segment.

The rapid (2 min) nongenomic effects of aldosterone (ALDO) and/or spironolactone (MR antagonist), RU 486 (GR antagonist), atrial natriuretic peptide (ANP) and dimethyl-BAPTA (BAPTA) on the intracellular pH recovery rate (pHirr) via NHE1 (basolateral Na⁺/H⁺ exchanger isoform), after the acid load induced by NH4Cl, and on the cytosolic free calcium concentration ([Ca²âº](i)) were investigated in the proximal S3 segment isolated from rats, by the probes BCECF-AM and FLUO-4-AM, respectively. The basal pHi was 7.15±0.008 and the basal pHirr was 0.195±0.012 pH units/min (number of tubules/number of tubular areas=16/96). Our results confirmed the rapid biphasic effect of ALDO on NHE1: ALDO (10⁻¹² M) increases the pHirr to approximately 59% of control value, and ALDO (10⁻6 M) decreases it to approximately 49%. Spironolactone did not change these effects, but RU 486 inhibited the stimulatory effect and maintained the inhibitory effect. ANP (10⁻6 M) or BAPTA (5×10⁻5 M) alone had no significant effect on NHE1 but prevented both effects of ALDO on this exchanger. The basal [Ca²âº](i) was 104±3 nM (15), and ALDO (10⁻¹² or 10⁻6 M) increased the basal [Ca²âº](i) to approximately 50% or 124%, respectively. RU 486, ANP and BAPTA decreased the [Ca²âº](i) and inhibited the stimulatory effect of both doses of ALDO. The results suggest the involvement of GR on the nongenomic effects of ALDO and indicate a pHirr-regulating role for [Ca²âº](i) that is mediated by NHE1, stimulated/impaired by ALDO, and affected by ANP or BAPTA with ALDO. The observed nongenomic hormonal interaction in the S3 segment may represent a rapid and physiologically relevant regulatory mechanism in the intact animal under conditions of volume alterations.

Genomic and nongenomic stimulatory effect of aldosterone on H+-ATPase in proximal S3 segments.

The genomic and nongenomic effects of aldosterone on the intracellular pH recovery rate (pHirr) via H(+)-ATPase and on cytosolic free calcium concentration ([Ca(2+)](i)) were investigated in isolated proximal S3 segments of rats during superfusion with an Na(+)-free solution, by using the fluorescent probes BCECF-AM and FLUO-4-AM, respectively. The pHirr, after cellular acidification with a NH(4)Cl pulse, was 0.064 ± 0.003 pH units/min (n = 17/74) and was abolished with concanamycin. Aldosterone (10(-12), 10(-10), 10(-8), or 10(-6) M with 1-h or 15- or 2-min preincubation) increased the pHirr. The baseline [Ca(2+)](i) was 103 ± 2 nM (n = 58). After 1 min of aldosterone preincubation, there was a transient and dose-dependent increase in [Ca(2+)](i) and after 6-min preincubation there was a new increase in [Ca(2+)](i) that persisted after 1 h. Spironolactone [mineralocorticoid (MR) antagonist], actinomycin D, or cycloheximide did not affect the effects of aldosterone (15- or 2-min preincubation) on pHirr and on [Ca(2+)](i) but inhibited the effects of aldosterone (1-h preincubation) on these parameters. RU 486 [glucocorticoid (GR) antagonist] and dimethyl-BAPTA (Ca(2+) chelator) prevented the effect of aldosterone on both parameters. The data indicate a genomic (1 h, via MR) and a nongenomic action (15 or 2 min, probably via GR) on the H(+)-ATPase and on [Ca(2+)](i). The results are compatible with stimulation of the H(+)-ATPase by increases in [Ca(2+)](i) (at 10(-12)-10(-6) M aldosterone) and inhibition of the H(+)-ATPase by decreases in [Ca(2+)](i) (at 10(-12) or 10(-6) M aldosterone plus RU 486).

Genomic and nongenomic dose-dependent biphasic effect of aldosterone on Na+/H+ exchanger in proximal S3 segment: role of cytosolic calcium.

The effects of aldosterone on the intracellular pH recovery rate (pHirr) via Na+/H+ exchanger and on the [Ca2+]i were investigated in isolated rat S3 segment. Aldosterone [10(-12), 10(-10), or 10(-8) M with 1-h, 15- or 2-min preincubation (pi)] caused a dose-dependent increase in the pHirr, but aldosterone (10(-6) M with 1-h, 15- or 2-min pi) decreased it (these effects were prevented by HOE694 but not by S3226). After 1 min of aldosterone pi, there was a transient and dose-dependent increase of the [Ca2+]i and after 6-min pi there was a new increase of [Ca2+]i that persisted after 1 h. Spironolactone, actinomycin D, or cycloheximide did not affect the effects of aldosterone (15- or 2-min pi) but inhibited the effects of aldosterone (1-h pi) on pHirr and on [Ca2+]i. RU 486 prevented the stimulatory effect of aldosterone (10(-12) M, 15- or 2-min pi) on both parameters and maintained the inhibitory effect of aldosterone (10(-6) M, 15- or 2-min pi) on the pHirr but reversed its stimulatory effect on the [Ca2+]i to an inhibitory effect. The data indicate a genomic (1 h, via MR) and a nongenomic action (15 or 2 min, probably via GR) on [Ca2+]i and on the basolateral NHE1 and are compatible with stimulation of the NHE1 by increases in [Ca2+]i in the lower range (at 10(-12) M aldosterone) and inhibition by increases at high levels (at 10(-6) M aldosterone) or decreases in [Ca2+]i (at 10(-6) M aldosterone plus RU 486).