RGD Reference Report - Heart rate and blood pressure quantitative trait loci for the airpuff startle reaction. - Rat Genome Database

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Heart rate and blood pressure quantitative trait loci for the airpuff startle reaction.

Authors: Jaworski, RL  Jirout, M  Closson, S  Breen, L  Flodman, PL  Spence, MA  Kren, V  Krenova, D  Pravenec, M  Printz, MP 
Citation: Jaworski RL, etal., Hypertension 2002 Feb;39(2 Pt 2):348-52.
RGD ID: 625381
Pubmed: PMID:11882571   (View Abstract at PubMed)

The airpuff startle reaction is a probe of sensori-autonomic processing and is useful for studies of genetic control of stress-induced cardiovascular activity. Using a Wistar-Kyoto-Spontaneously Hypertensive Rat F2 cross, we reported an airpuff-elicited strain-dependent and trial-dependent bradycardia, the absence of which cosegregated with hypertension. Here, we use the mapping power of the HXB-BXH recombinant inbred rat strains (n=23) to locate quantitative trait loci (QTL) for this and associated cardiovascular phenotypes. Rats (12 weeks old), with indwelling femoral arterial catheters, were subjected to repeated airpuff startle stimuli (100 ms, 12.5 psi, 28 trials). Basal mean arterial pressure (MAP), delta MAP, and delta heart rate response to airpuff stimuli were analyzed as the average over 28 trials. There was a significant strain effect on the cardiovascular phenotypes measured. One QTL for the bradycardia elicited by the first airpuff stimulus was identified on chromosome 2 (D2rat 62/63; logarithm of odds [LOD] 2.9) mapping near a reported blood pressure locus. Further QTL were identified for basal MAP (RN08), stimulus-elicited tachycardia on trials 2 to 5 (RNO1 and RNO10), and delta MAP (RNO6). Our results indicate that chromosomes 1, 2, and 10 are involved in heart rate responses to airpuff startle stimulus, and chromosomes 6 and 8 are involved in pressor responses. This study is the first to identify stress-related heart rate loci and provides additional support for our prior cosegregation results. Furthermore, we have established the utility of this experimental paradigm to identify loci responsible for cardiovascular regulation during stress in genetic hypertensive models.

RGD Manual Disease Annotations    Click to see Annotation Detail View

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Hrtrt19RatBradycardia  IAGP  RGD 
Hrtrt19Ratheart disease  IAGP  RGD 
Hrtrt20Ratheart disease  IAGP  RGD 
Hrtrt21Ratheart disease  IAGP  RGD 
Bp271Rathypertension  IAGP  RGD 
Bp272Rathypertension  IAGP  RGD 

Phenotype Annotations    Click to see Annotation Detail View

Mammalian Phenotype

Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Hrtrt19Ratdecreased heart rate  IAGP  RGD 
Bp271Ratdecreased systemic arterial blood pressure  IAGP  RGD 
Bp272Ratdecreased systemic arterial blood pressure  IAGP  RGD 
Hrtrt20Ratincreased heart rate  IAGP  RGD 
Hrtrt21Ratincreased heart rate  IAGP  RGD 
Objects Annotated

Bp271  (Blood pressure QTL 271)
Bp272  (Blood pressure QTL 272)
Hrtrt19  (Heart rate QTL 19)
Hrtrt20  (Heart rate QTL 20)
Hrtrt21  (Heart rate QTL 21)

BXH/Ipcv  (NA)
HXB/Ipcv  (NA)

Additional Information