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RESEARCH: Hugh Tunstall-Pedoe, John Connaghan, Mark Woodward, Hanna Tolonen, and Kari Kuulasmaa Pattern of declining blood pressure across replicate population surveys of the WHO MONICA project, mid-1980s to mid-1990s, and the role of medication BMJ 2006; 332: 629-635 [Abstract] [Full text]

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Angiotensin II type I receptor gene polymorphism and hypertension

Prasanta Padhan   (18 March 2006)

Alcohol

Richard Frank Gunstone   (24 March 2006)

Age or year of birth?

Tom Hughes-Davies   (25 March 2006)

Effect of Global Warming

Murali Vallipuranathan   (28 March 2006)

Mass population change may mimic treatment effect

Arnaud Chiolero, Nadia Danon   (17 May 2006)

Angiotensin II type I receptor gene polymorphism and hypertension 18 March 2006
Prasanta Padhan, MD,SENIOR RESIDENT IN INTERNAL MEDICINE JIPMER,PONDICHERRY,INDIA.605006 Send response to journal: Re: Angiotensin II type I receptor gene polymorphism and hypertension	Dear Editor, The genetic determinants play an important role in blood pressure in the population.One of the most important physiological pathways affecting the cardiovascular system and fluid and electrolyte balance is the renin angiotensin system (RAS) which, in parallel with kinins, has diverse regulatory roles in vasoconstriction, cell proliferation, and secretion of aldosterone from the adrenal gland.The genetic diversity of the RAS pathway impact on vascular traits of the individual.Angiotensin II (AGT II) is the central component of the RAS pathway. It acts through two main receptors: the angiotensin II type I receptor (AGTR1 or AT1R) and the angiotensin II type II receptor (AGTR2). It is generally believed that AGTR1 is the dominant receptor in the cardiovascular system.Angiotensin II type I receptor (AGTR1) A1166C genotype has been found to be associated with the development of hypertension and coronary disease. Reference: van Geel PP, Pinto YM, Voors AA, Buikema H, Oosterga M, Crijns HJ, van Gilst WH. Angiotensin II type 1 receptor A1166C gene polymorphism is associated with an increased response to angiotensin II in human arteries. Hypertension 2000;35 (3) :717–721. Competing interests: None declared
Alcohol 24 March 2006
Richard Frank Gunstone, Lecturer in undrgraduate medicine. Retired Consultan Physician Walsgrave Hopital CV2 2DX Send response to journal: Re: Alcohol	It is just possible that some people are drinking less. I can't recall hearing about alcohol as a risk factor for hypertension till 10 to 20 years ago. Competing interests: We will all be safer if alcohol consumption goes down, but not to zero
Age or year of birth? 25 March 2006
Tom Hughes-Davies, Paediatrician Breamore Marsh SP6 2EJ Send response to journal: Re: Age or year of birth?	Though the ages of the populations in successive decades were the same, one was born in about 1921-1950 and the other in 1931-1960. Their care before and after birth, their diet, vaccination, and experience of infection, war, famine or plenty may have differed considerably. It would be interesting to examine changes in blood pressure by year of birth as well as by age. Competing interests: None declared
Effect of Global Warming 28 March 2006
Murali Vallipuranathan, Senior Registrar (Community Medicine) Ministry of Health Care, 385, Deans Road, Colombo-10, Sri Lanka Send response to journal: Re: Effect of Global Warming	Hugh Tunstall-Pedoe et al implied that factors other than the antihypertensive treatment were more pervasive and powerful in lowering blood pressure across the whole populations from mid-1980s to mid-1990s (1). In this context, effect of global warming must be considered as a possible factor that could have contributed to the lowering of blood pressure of the whole population. Environmental temperature is known to have an inverse relationship with blood pressure (2). The difference between summer and winter temperatures in Britain results in a difference of about 5 mm Hg in blood pressure (3). The differences in mean blood pressure observed between mid-1980s and mid-1990s were smaller than 5mm Hg (1). Therefore analysis should be made with respect to the mean environmental temperatures of the studied countries in mid-1980s and mid- 1990s. Attention should also focus on whether blood pressure recordings were made during the same season in mid-1980s and mid-1990s. References 1. Hugh Tunstall-Pedoe, John Connaghan, Mark Woodward, Hanna Tolonen, Kari Kuulasmaa. Pattern of declining blood pressure across replicate population surveys of the WHO MONICA project, mid-1980s to mid-1990s, and the role of medication, BMJ 2006; 332: 629-635 2. Kunes J, Tremblay J, Bellavance F, Hamet P. Influence of environmental temperature on the blood pressure of hypertensive patients in Montreal. American Journal of Hypertension 1991;4:422-6. 3. Wilmshurst P. Temperature and cardiovascular mortality BMJ, Oct 1994; 309: 1029 - 1030 Competing interests: None declared
Mass population change may mimic treatment effect 17 May 2006
Arnaud Chiolero, research fellow University Institute of Social and Preventive Medicine, 1004 Lausanne, Switzerland, Nadia Danon Send response to journal: Re: Mass population change may mimic treatment effect	To the editor, We fully agree with Tunstall-Pedoe et al. that the decrease in blood pressure in the populations surveyed in the WHO MONICA project is likely to reflect a population-wide change rather than an improvement in antihypertensive treatment (1). However, their assumption stating that a decline restricted to high readings would be the result of better antihypertensive treatment goes too far : as a matter of fact, a decline in the upper part of the tail would also be compatible with a mass population change. Let’s suppose that salt intake has decreased in the surveyed populations throughout this decade. Individuals’ response to a decline in salt intake is not homogeneous: among “salt-sensitive” individuals, reducing salt intake results in a large decrease of blood pressure, while among “salt resistant” individuals, blood pressure does not change (2, 3). Individuals with elevated blood pressure tend to be more frequently salt- sensitive than individuals with normal blood pressure, for whom a decrease in salt intake only results in a slight decrease in blood pressure (4). Therefore, were salt intake reduced at a population level, one would not expect a uniform reduction throughout the blood pressure distribution. It would result in a more pronounced decline in high readings compared to middle or low readings. In such a case, it could not be distinguished from the effects of antihypertensive treatment at a population level. 1) Tunstall-Pedoe H et al. Pattern of declining blood pressure across replicate population surveys of the WHO MONICA project, mid-1980s to mid- 1990s, and the role of medication. BMJ 2006; 332: 629-35. 2) Chiolero A et al. Renal determinants of the salt sensitivity of blood pressure. Nephrol Dial Transplant 2001; 16: 452-8. 3) Johnson RJ et al. Subtle acquired renal injury as a mechanism of salt- sensitive hypertension. N Engl J Med 2002; 346: 913-23. 4) He FJ, MacGregor GA. Effect of longer-term modest salt reduction on blood pressure. Cochrane Database Syst Rev 2004; 3: CD004937. Competing interests: None declared